AntiCan Cancer Research Results

AntiCan, Anticancer Effect: Click to Expand ⟱
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Anticancer Effect


Scientific Papers found: Click to Expand⟱
4384- ,    Silver nanoparticles: synthesis, properties, and therapeutic applications
- Review, Var, NA
AntiCan↑, AgNPs are employed in newly emerging applications as photosensitizers/radiosensitizers, antiviral and anticancer agents.
RadioS↑,
CellMemb↑, underlying anticancer mechanisms of AgNPs include (1) disruption of cell membranes, and (2) production of reactive oxygen species and Ag+ to damage protein or DNA.
ROS↑,
DNAdam↑,
PhotoS↑, photosensitizing mechanism of AgNPs is based on nonradiative decay converting photo energy to thermal energy.
eff↑, Smaller particles have a larger surface area and, therefore, have greater toxic potential

4442- ,    Anticancer and Hepatoprotective Role of Selenium Nanoparticles against
- in-vivo, Liver, HepG2 - NA, Nor, NA
*hepatoP↑, histopathological studies indicated that the liver acrylamide induced in mice showed necrosis and damage in liver cells, but the treatment of mice with SeNPs, reduced the effect of acrylamide significantly.
AntiCan↑, green synthesized SeNPs exhibit both in vitro and in vivo anticancer and hepatoprotective effects

5275- 3BP,    3-Bromopyruvate (3BP) a fast acting, promising, powerful, specific, and effective "small molecule" anti-cancer agent taken from labside to bedside: Introduction to a special issue
- Review, Var, NA
AntiCan↑, the subject of this mini-review series, is an incredibly powerful and swift acting anticancer agent.
HK2↓, reported that HK2 is constitutively overexpressed and that 3BP an inhibitor of this enzyme induces cell death.
OCR↓, this agent was found to inhibit the membrane potential, oxygen consumption, and dehydrogenase activities.

5273- 3BP,    The promising anticancer drug 3-bromopyruvate is metabolized through glutathione conjugation which affects chemoresistance and clinical practice: An evidence-based view
- Review, Var, NA
AntiCan↑, 3BP exhibited strong anticancer effects in both preclinical and human studies e.g. energy depletion, oxidative stress, anti-angiogenesis, anti-metastatic effects, targeting cancer stem cells and antagonizing the Warburg effect.
ROS↑,
angioG↓,
CSCs↓,
Warburg↓,
GSH↓, Reported decrease in endogenous cellular GSH content upon 3BP treatment was confirmed to be due to the formation of 3BP-GSH complex i
Thiols↓, Being a thiol blocker, 3BP may attack thiol groups in tissues and serum proteins e.g. albumin and GSH.

4774- 5-FU,  TQ,  CoQ10,    Exploring potential additive effects of 5-fluorouracil, thymoquinone, and coenzyme Q10 triple therapy on colon cancer cells in relation to glycolysis and redox status modulation
- in-vitro, CRC, NA
AntiCan↑, All treatments resulted in anticancer effects depicted by cell cycle arrest and apoptosis, with TQ demonstrating greater efficacy than CQ10, both with and without 5-FU.
TumCCA↑,
Apoptosis↑,
eff↑,
Bcl-2↓, However, 5-FU/TQ/CQ10 triple therapy exhibited the most potent pro-apoptotic activity in all cell lines, portrayed by the lowest levels of oncogenes (CCND1, CCND3, BCL2, and survivin)
survivin↓,
P21↑, and the highest upregulation of tumour suppressors (p21, p27, BAX, Cytochrome-C, and Cas- pase-3).
p27↑,
BAX↑,
Cyt‑c↑,
Casp3↑,
PI3K↓, The triple therapy also showed the strongest suppression of the PI3K/AKT/mTOR/HIF1α pathway, with a concurrent increase in its endogenous inhibitors (PTEN and AMPKα) in all cell lines used.
Akt↓,
mTOR↓,
Hif1a↓,
PTEN↑,
AMPKα↑,
PDH↑, triple therapy favoured glucose oxidation by upregulating PDH, while decreasing LDHA and PDHK1 enzymes.
LDHA↓,
antiOx↓, most significant decline in antioxidant levels and the highest increases in oxidative stress markers
ROS↑,
AntiCan↑, This study is the first to demonstrate the superior anticancer effects of TQ compared to CQ10, with and without 5-FU, in CRC treatment.

5472- AF,    Auranofin induces apoptosis and necrosis in HeLa cells via oxidative stress and glutathione depletion
- in-vitro, Cerv, HeLa
TrxR↓, Auranofin (Au), an inhibitor of thioredoxin reductase, is a known anti‑cancer drug
AntiCan↑,
TumCG↓, Au inhibited the growth of HeLa cells with an IC50 of ~2 µM at 24 h.
Apoptosis↑, This agent induced apoptosis and necrosis, accompanied by the cleavage of poly (ADP‑ribose) polymerase and loss of mitochondrial membrane potential.
necrosis↑,
cl‑PARP↑,
MMP↓,
ROS↑, With respect to the levels of ROS and GSH, Au increased intracellular O2•- in the HeLa cells and induced GSH depletion.
GSH↓,
eff↓, The antioxidant, N‑acetyl cysteine, not only attenuated apoptosis and necrosis in the Au‑treated HeLa cells, but also decreased the levels of O2•- and GSH depletion in the cells.

5434- AG,    Recent Advances in the Mechanisms and Applications of Astragalus Polysaccharides in Liver Cancer Treatment: An Overview
- Review, Liver, NA
AntiCan↑, Preclinical studies indicate that APS exerts significant anti-liver cancer effects through multiple biological actions, including the promotion of apoptosis, inhibition of proliferation, suppression of epithelial–mesenchymal transition, regulation of
Apoptosis↑,
TumCP↓,
EMT↓,
Imm↑, improving host immune response
ChemoSen↑, APS exhibits synergistic effects when combined with conventional chemotherapeutics and interventional treatments such as transarterial chemoembolisation, improving efficacy and reducing toxicity.
BioAv↓, limitations such as low bioavailability and a lack of large-scale clinical trials remain challenges for clinical translation.
TumCG↓, APS significantly inhibited tumour growth in H22-bearing mice with a dose-dependent effect (100, 200, 400 mg/kg), with the 400 mg/kg group achieving a tumour inhibition rate of 59.01%
IL2↑, APS enhance the thymus and spleen indices and elevates the key cytokines, including IL-2, IL-12, and TNF-α.
IL12↑,
TNF-α↑,
P-gp↓, APS reversed chemoresistance by downregulating P-glycoprotein and MDR1 mRNA expression
MDR1↓,
QoL↑, These effects contributed to improved treatment tolerance and enhanced quality of life [39].
Casp↑, APS can activate both the intrinsic and extrinsic apoptotic pathways, leading to caspase activation and DNA fragmentation
DNAdam↑,
Bcl-2↓, Mechanistically, APS downregulate antiapoptotic proteins such as Bcl-2 while upregulating proapoptotic proteins such as Bax and cleaved caspase-3.
BAX↑,
MMP↓, APS have been shown to disrupt the mitochondrial membrane potential and promote the release of cytochrome c, thereby enhancing apoptotic cascades in hepatocellular carcinoma models.
Cyt‑c↑,
NOTCH1↓, APS (0.1, 0.5, and 1.0 mg/mL) were shown to reduce both mRNA and protein levels of Notch1 in a concentration-dependent manner.
GSK‐3β↓, APS significantly inhibited the proliferation of HepG2 cells by downregulating the expression of glycogen synthase kinase-3β (GSK-3β), with 200 μg/mL being the most effective concentration.
TumCCA↑, APS exerted these effects by inducing cell cycle arrest at the G2/M and S phases, thereby impeding tumour cell proliferation [35].
GSH↓, HepG2 cells. APS also reduced intracellular glutathione (GSH) levels, increased reactive oxygen species (ROS) and lipid peroxidation levels, and elevated intracellular iron ion concentrations—all in a dose-dependent manner.
ROS↑,
lipid-P↑,
c-Iron↑,
GPx4↓, APS treatment led to the downregulation of GPX4 and upregulation of ACSL4, indicating that APS promotes ferroptosis in liver cancer cells.
ACSL4↑,
Ferroptosis↑,
Wnt↓, inhibit the expression of key proteins involved in the Wnt/β-catenin signalling pathway
β-catenin/ZEB1↓,
cycD1/CCND1↓, by downregulating the key oncogenic targets, including β-catenin, C-myc, and cyclin D1, which subsequently reduces Bcl-2 expression and activates the apoptotic cascade in HepG2 liver cancer cells.
Akt↓, It also inhibited the Akt/p-Akt signalling pathway.
PI3K↓, APS inhibit the PI3K/AKT/mTOR signalling pathway, which is a central negative regulator of autophagy.
mTOR↓,
CXCR4↓, PS upregulated the epithelial marker E-cadherin while downregulating the mesenchymal marker vimentin and the chemokine receptor CXCR4 at both mRNA and protein levels, suggesting that APS suppress liver cancer cell growth and metastasis by inhibiting
Vim↓,
PD-L1↓, APS interfere with immune checkpoint signalling by downregulating Programmed death-ligand 1 (PD-L1) expression on tumour cells.
eff↑, The preparation of polysaccharide–SeNP composites typically involves using sodium selenite (Na2SeO3) as the precursor and ascorbic acid (Vc) as the reducing agent, with synthesis carried out via a chemical reduction method in a polysaccharide solutio
eff↑, Mechanistic investigations revealed that AASP–SeNPs elevated intracellular ROS levels and reduced the mitochondrial membrane potential (∆Ψm).
ChemoSen↑, APS enhance doxorubicin-induced endoplasmic reticulum (ER) stress by reducing O-GlcNAcylation levels, thereby promoting apoptosis of liver cancer cells.
ChemoSen↑, APS inhibited BEL-7404 human liver cancer cell growth in a concentration-dependent manner and showed stronger cytotoxicity when combined with cisplatin.
chemoP↑, APS protects against chemotherapy-induced liver injury, particularly that caused by CTX, through antiapoptotic mechanisms

5976- AgNPs,    Review on Harnessing Silver Nanoparticles for Therapeutic Innovations: A Comprehensive Review on Medical Applications, Safety, and Future Directions
- Review, Vit, NA
*Bacteria↓, strong antibacterial, anticancer, anti-inflammatory, and wound-healing properties.
AntiCan↑,
*Inflam↓,
*Wound Healing↑,
eff↑, Cytotoxic effects of anticancer drugs such as verapamil, cisplatin, carmustine, and methotrexate are improved by citrate-coated silver oxide NP
ChemoSen↑,
EGFR↓, silver (AgNPs), gold (AuNPs), and superparamagnetic iron oxide nanoparticles (SPIONPs) have shown the ability to interfere with EGFR
ROS↑, In MCF-7 breast cancer cells, AgNP induced ROS activated proteins, such as p53, Bax, and caspase-3, cause programmed cell death
P53↑,
BAX↑,
Casp3↑,
toxicity↝, AgNPs produce ionic silver and ROS that have antibacterial properties, but their non-specific absorption can harm healthy cells.

5978- AgNPs,    Biological synthesis of silver nanoparticles and their medical applications
- Review, Var, NA
Wound Healing↑, The notable antimicrobial properties of silver render it indispensable for wound healing, infection control, cancer therapy and tissue regeneration applications.
AntiCan↑,
other↑, Additionally, AgNPs hold great promise as versatile drug carriers for targeted therapies and as contrast agents for advanced medical imaging techniques
MPT↑, these nanoparticles exert their effects by disrupting cell membrane permeability, interfering with cellular respiration processes and instigating the production of free radicals.
ROS↑,
other↑, Additionally, it has been proposed that AgNPs may release silver ions, which can bind to thiol groups found in essential enzymes, rendering them inactive
DNAdam↑, DNA typically contains sulfur, and nanoparticles may interact with these bases, potentially causing damage to the DNA molecule, and thereby contributing to cell demise

4403- AgNPs,    Silver Nanoparticles Decorated UiO-66-NH2 Metal-Organic Framework for Combination Therapy in Cancer Treatment
- in-vitro, GBM, U251 - in-vitro, GBM, U87MG - in-vitro, GBM, GL26 - in-vitro, Cerv, HeLa - in-vitro, CRC, RKO
AntiCan↑, Among the various NPs, silver nanoparticles (AgNPs) have garnered attention due to their cytotoxic and genotoxic properties in cancer cells.
eff↑, Our results demonstrate that UiO-66-NH2@AgNPs@Cis-Pt and its combinations exhibit enhanced cytotoxicity compared to individual components such as AgNPs and Cis-Pt.
EPR↑, Their nanometric structure allows them to easily penetrate and accumulate in tumour tissues either actively, via targeting systems [6,7,8], or passively, by taking advantage of tumour angiogenesis and the enhanced permeation and retention (EPR) effe
selectivity↑,
ROS↑, Once inside, AgNPs induce an increase in the production of reactive oxygen species (ROS) and cause mitochondrial dysfunctions, caspases activation, apoptosis, autophagy, and DNA damage
Casp↑,
Apoptosis↑,
DNAdam↑,
tumCV↓, figure 8
eff↑, One of the primary characteristics of AgNPs is their ability to release Ag+ ions from their surface in response to low pH or oxidation.

4396- AgNPs,    Identification of possible reductants in the aqueous leaf extract of mangrove plant Rhizophora apiculata for the fabrication and cytotoxicity of silver nanoparticles against human osteosarcoma MG-63 cells
- in-vitro, OS, MG63
AntiCan↑, Tannins have been known to reduce silver ions into silver nanoparticles which in particular are known to possess cytotoxic effects against a variety of cancer cells.
tumCV↓, nanoparticles possessed significant cytotoxic effects against MG-63 cells which could be possibly attributed to the antioxidant activity of silver nanoparticles.

4389- AgNPs,    Graphene Oxide-Silver Nanocomposite Enhances Cytotoxic and Apoptotic Potential of Salinomycin in Human Ovarian Cancer Stem Cells (OvCSCs): A Novel Approach for Cancer Therapy
- in-vitro, Ovarian, NA
tumCV↓, Ag was toxic to OvCSCs and reduced cell viability by mediating the generation of reactive oxygen species, leakage of lactate dehydrogenase, reduced mitochondrial membrane potential
ROS↑,
LDH↓,
MMP↑,
CSCs↓, rGO–Ag may be a novel nano-therapeutic molecule for specific targeting of highly tumorigenic ALDH+CD133+ cells
AntiCan↑, Overall, these results suggest that the rGO–Ag is a promising material for inhibiting the cell viability of ovarian cancer cells and ovarian cancer stem cells.

4422- AgNPs,    Bioengineering of Piper longum L. extract mediated silver nanoparticles and their potential biomedical applications
- in-vitro, Cerv, HeLa
AntiCan↑, Anticancer activity revealed the strong and dose-dependent cytotoxic effect of AgNPs against the HeLa cells showing maximum IC50 value being 5.27 μg/mL after 24 h
selectivity↑, was also found to be non-toxic to normal cells (HEK)

4412- AgNPs,    Biosynthesis and characterization of silver nanoparticles from Asplenium dalhousiae and their potential biological properties
- in-vitro, CRC, HCT116 - in-vitro, Melanoma, A2780S
Bacteria↓, The antioxidant activity of the synthesized AgNPs was assessed using the DPPH method, which confirmed their significant antioxidant properties alongside their antibacterial activity.
antiOx↑, AgNPs but also exhibits substantial antioxidant properties
AntiCan↑, anticancer activities
eff↑, The combination of Asplenium dalhousiae leaf methanolic extracts and synthesized silver nanoparticles (AgNPs: aqueous, n-hexane, and CHCl3 fractions) exhibits varied apoptotic activity against ovarian and colorectal cancer cells.

4411- AgNPs,    Eco-friendly synthesis of silver nanoparticles using Anemone coronaria bulb extract and their potent anticancer and antibacterial activities
- in-vitro, Lung, A549 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, PC3 - in-vitro, Nor, HEK293
AntiCan↑, (AgNPs) have emerged as promising multifunctional agents in biomedical applications due to their notable antimicrobial and anticancer properties.
selectivity↑, demonstrated significant cytotoxic effects on cancer cells while sparing normal cells
Apoptosis↑, Apoptosis induction, cell cycle arrest, and gene expression analyses further validated their anticancer efficacy.
TumCCA↑,
Bacteria↓, Figure 6a,b show the inhibition zones of 10 µg ampicillin and 10, 50, 100, and 150 μg/mL AgNPs against bacteria on agar for two repeated tests.
tumCV↓, AgNPs at concentrations of 6.3, 6.8, 7.5, 8.3, 9.4, 10.7 and 12.5 µg/mL for 24 h. After treatment, a significant decrease in cell viability was observed in different cancer cell types,
selectivity↑, The toxic effect was weaker in healthy cells than in cancer cells
Apoptosis↑, Fig. 8a–c, a significant increase (p < 0.01; p < 0.001) in the rate of early and late apoptotic cells was observed in A549, MIA PaCa-2 and PC-3 cells.
TumCCA↑, accompanied by arrest in the S phase and, particularly, the G2/M phase.

4410- AgNPs,    Green-synthesized silver nanoparticles: a sustainable nanoplatform for targeted colon cancer therapy
- Review, Colon, NA
AntiCan↑, AgNPs exert potent anticancer effects against colon cancer cell lines primarily by inducing cell death through mechanisms including reactive oxygen species (ROS) generation
ROS↑,
mtDam↑, mitochondrial dysfunction, and apoptosis modulation, leading to significant reductions in cell viability.
tumCV↓,
selectivity↑, effectively targeting cancer cells while sparing healthy counterparts, thereby emphasizing their safety profile and potential for minimizes ng systemic toxicity.

4431- AgNPs,  doxoR,    Oxidative Stress-Induced Silver Nano-Carriers for Chemotherapy
- in-vitro, BC, 4T1 - in-vivo, BC, 4T1 - in-vitro, Nor, 3T3
AntiCan↑, AgNPs have been demonstrated to exhibit anti-tumor effects through cell apoptosis.
ROS↑, ox-carried PA-AgNPs generate reactive oxidation species intensively beside 4T1 cells.
TumVol↓, in vivo study confirms that PA-AgNPs with Dox successfully inhibit tumors, which are about four times smaller than the control group and have high biosafety that can be applied for chemotherapy.
EPR↑, While all normal cells need enough vitamins to survive, cancer cells require a considerable number of vitamins to proliferate rapidly. As a result, the receptors on the cancer cell surface are overexpressed to capture as many vitamins as possible.
selectivity↑, PA-AgNPs (without/with Dox) concentrations ranging from 0 to 100 μg mL−1 did not seem to impair 3T3 cell viability due to poor uptake by normal cells.
ChemoSen↑, These results suggested that Dox-carried PA-AgNPs were both safer and more effective for cancer prevention.

4552- AgNPs,  ART/DHA,    Green synthesis of silver nanoparticles using Artemisia turcomanica leaf extract and the study of anti-cancer effect and apoptosis induction on gastric cancer cell line (AGS)
- in-vitro, GC, AGS
AntiCan↑, iologically synthesized silver nanoparticles induced apoptosis, and showed a cytotoxic and anti-cancer effect against gastric cancer cell lines in a dose- and time-dependent manner.
Apoptosis↑,
eff↑, Biologically synthesized nanoparticles may possess higher anti-cancer properties than commercial silver

4561- AgNPs,  VitC,    Cellular Effects Nanosilver on Cancer and Non-cancer Cells: Potential Environmental and Human Health Impacts
- in-vitro, CRC, HCT116 - in-vitro, Nor, HEK293
NRF2↑, Nanosilver increased Nrf2 protein expression and disrupted the cell cycle at the G1 and G2/M phases.
TumCCA↑, AgNPs interact with DNA to stop the cell cycle and lead to apoptosis
ROS↑, Nanosilver induced significant mitochondrial oxidative stress in HCT116, whereas it did not in the non-cancer HIEC-6 and nanosilver/sodium ascorbate co-treatment was preferentially lethal to HCT116 cells,
selectivity↑,
*AntiViral↑, AgNPs are effective antiviral agents against various viruses such as human immunodeficiency virus, hepatitis B virus, and monkey pox virus through interaction with surface glycoproteins on the virus
*toxicity↝, Citrate and PVP-coated AgNPs have been found to be less toxic than non-coated AgNPs
ETC↓, AgNPs affects mitochondrial function through the disruption of the electron transport chain2,24,26,33,39–41
MMP↓, Studies have shown that exposure to AgNPs resulted in a decrease of mitochondrial membrane potential (MMP) in various in vitro and in vivo experiments
DNAdam↑, AgNPs has also been shown to interact with and induce damage to DNA, DNA strand breaks, DNA damage
Apoptosis↑, apoptosis induced by AgNPs were through membrane lipid peroxidation, ROS, and oxidative stress
lipid-P↑,
other↝, Several studies have showed AgNPs interact with various proteins such as haemoglobin, serum albumin, metallothioneins, copper transporters, glyceraldehyde 3-phosphate dehydrogenase (GAPDH), malate dehydrogenase (MDH), and bacterial proteins.
UPR↑, Studies have shown exposure to AgNPs induces activation of the UPR
*GRP78/BiP↑, AgNPs induced increased levels of GRP78, phosphorylated PERK, phosphorylated eIF2-α, and phosphorylated IRE1α, spliced XBP1, cleaved ATF-6, CHOP, JNK and caspase 12
*p‑PERK↑,
*cl‑eIF2α↑,
*CHOP↑,
*JNK↑,
Hif1a↓, One study showed AgNPs inhibits HIF-1 accumulation and suppresses expression of HIF-1 target genes in breast cancer cells (MCF-7) and also found the protein levels of HIF-1α and HIF-1β decreased
AntiCan↑, Many studies have shown that ascorbic acid, on its own, has anti-cancer effects
*toxicity↓, However, when the rats were treated with both ascorbic acid and AgNPs, a decrease in toxic effects was observed in non-cancer parotid glands in rats
eff↑, Studies have shown both AgNPs and ascorbic acid have greater effects and toxicity in cancer cells relative to non-cancer cells

4560- AgNPs,    Exploiting antidiabetic activity of silver nanoparticles synthesized using Punica granatum leaves and anticancer potential against human liver cancer cells (HepG2)
- in-vitro, Liver, HepG2 - in-vitro, Diabetic, NA
AntiCan↑, The PGE-AgNPs showed a dose-dependent response against human liver cancer cells (HepG2) (IC50; 70 μg/mL) indicating its greater efficacy in killing cancer cells.
Dose↝, surface charge of synthesized AgNPs was highly negative (−26.6 mV) and particle size distribution was ranging from ∼35 to 60 nm and the average particle size was about 48 nm determined by dynamic light scattering (DLS)
*antiOx↑, literature suggests that AgNPs display considerable antioxidant activity in vitro
*AntiDiabetic↑, Antidiabetic potential of biosynthesized AgNPs
*Bacteria↓, Synergistic antibacterial potential of AgNPs with standard antibiotics

4555- AgNPs,    Silver nanoparticles from Dendropanax morbifera Léveille inhibit cell migration, induce apoptosis, and increase generation of reactive oxygen species in A549 lung cancer cells
- in-vitro, Lung, A549 - in-vitro, Liver, HepG2
*Bacteria↓, silver nanoparticles synthesized from Dendropanax morbifera Léveille leaves (D-AgNPs) exhibit antimicrobial activity and reduce the viability of cancer cells without affecting the viability of RAW 264.7 macrophage-like cells
tumCV↓,
selectivity↑,
ROS↑, enhanced the production of ROS in both cell lines.
Apoptosis↑, An increase in cell apoptosis and a reduction in cell migration in A549 cells were also observed after D-AgNP treatment.
TumCMig↓,
AntiCan↑, potential of D-AgNPs as a possible anticancer agent, particularly for the treatment of non-small cell lung carcinoma.

4539- AgNPs,  VitC,  Citrate,    Investigating the Anti-cancer Potential of Silver Nanoparticles Synthesized by Chemical Reduction of AgNO3 Using Trisodium Citrate and Ascorbic Acid
- in-vitro, Nor, L929 - in-vitro, Ovarian, SKOV3
AntiCan↑, Significant cytotoxicity was observed in SKOV-3 ovarian cancer cells

4548- AgNPs,  Chit,    Synergistic combination of antioxidants, silver nanoparticles and chitosan in a nanoparticle based formulation: Characterization and cytotoxic effect on MCF-7 breast cancer cell lines
- in-vitro, BC, MCF-7
AntiCan↑, anti-cancer efficacy was observed against MCF-7 breast cancer cells having IC50 values of 53.36 ± 0.36 μg/mL (chitosan–ascorbic acid–glucose
EPR↑, we hypothesize that the nanoformulations can be up-taken readily by the cancer cells
pH↝, cancer cells are known to be acidic therefore the chitosan matrix can readily dissolve releasing the encapsulated components thereby triggering the subsequent death process in the cancerous cells

4542- AgNPs,    Silver Nanoparticles (AgNPs): Comprehensive Insights into Bio/Synthesis, Key Influencing Factors, Multifaceted Applications, and Toxicity─A 2024 Update
- Review, NA, NA
AntiCan↑, cytotoxicity against human colon carcinoma (HT-29) cells. The MTT assay confirmed their anticancer potential, with an IC50 value of 150.8 μg/mL.
DNAdam↑, Ag-NPs, accumulating in the nucleus, may cause genotoxicity, DNA damage, and chromosomal aberrations
ATP↓, Ag-NP exposure disrupts calcium homeostasis, leading to mitochondrial dysfunction, ATP depletion, and apoptosis.
Apoptosis↑,
ROS↓, induce cytotoxicity through numerous mechanisms viz., oxidative stress, mitochondrial dysfunction, DNA damage, cell cycle arrest, and subsequent apoptosis.
TumCCA↑,
*Bacteria↓, effectiveness as an antibacterial agent.
*BMD↑, Bone Repair Applications

4584- AgNPs,    Silver Nanoparticles Synthesized Using Carica papaya Leaf Extract (AgNPs-PLE) Causes Cell Cycle Arrest and Apoptosis in Human Prostate (DU145) Cancer Cells
- in-vitro, Pca, DU145
selectivity↑, AgNPs-PLE when compared with AgNPs-citric acid or PLE showed better efficacy against cancer cells and was also relatively less toxic to normal cells.
ROS↑, ROS production was observed at earlier time points in presence of AgNPs-PLE, suggesting its role behind apoptosis in DU145 cells.
BAX↑, induction of Bax, cleaved caspase-3, and cleaved PARP proteins. G1-S phase cell cycle check point marker, cyclin D1 was down-regulated along with an increase in cip1/p21 and kip1/p27 tumor suppressor proteins by AgNPs-PLE.
cl‑Casp3↑,
p‑PARP↑,
TumCCA↑,
cycD1/CCND1↓,
p27↑,
P21↑,
AntiCan↑, These findings suggest the anti-cancer properties of AgNPs-PLE.

5356- AL,    Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects
- Review, GC, NA
Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo

5354- AL,    Therapeutic Potential of Allicin-Rich Garlic Preparations: Emphasis on Clinical Evidence toward Upcoming Drugs Formulation
- Review, Var, NA
*LDL↓, Indeed, clinical studies on healthy subjects have evidenced that standardized garlic treatment (900 mg/day) significantly reduces total cholesterol (TC) and low-density lipoprotein cholesterol (c-LDL).
*antiOx↑, Multiple studies have focused on allicin therapeutic potential as an antioxidant (inducing antioxidant product production),
AntiCan↑, anticancer (triggering cancer cells apoptosis and inhibiting tumor growth),
*cardioP↑, cardioprotective (decreasing angiogenesis and inducing vasorelaxation)
*BP↓, Conversely, aged garlic extract supplementation was shown to be more effective than the placebo in lowering systolic blood pressure
*Weight↓, Garlic powder supplementation (800 mg/daily) resulted in a significant decrease in body weight and body fat mass (
NK cell↑, Actually, aged garlic administration in patients with advanced cancer of the digestive system led to an improvement of natural killer (NK) cell activity but did not cause improvement in QoL
*AntiDiabetic↑, Actually, daily garlic allicin supplementation (0.05–1.5 g) displayed a positive and sustained role in blood glucose, total cholesterol (TC), and high/low density lipoprotein (HDL-c/LDL-c) regulation in type 2 diabetes mellitus (T2DM) management
*GSH↑, 2-month application of coated garlic powder tablets (900 mg with alliin and allicin contents of 1.3% and 0.6%, respectively), the glutathione (GSH) concentration significantly increased in circulating human erythrocytes

2558- AL,    Allicin, an Antioxidant and Neuroprotective Agent, Ameliorates Cognitive Impairment
- Review, AD, NA
*AntiCan↑, Allicin has shown anticancer, antimicrobial, antioxidant properties and also serves as an efficient therapeutic agent against cardiovascular diseases
*antiOx↑,
*cardioP↑,
*neuroP↑, present review describes allicin as an antioxidant, and neuroprotective molecule
cognitive↑, that can ameliorate the cognitive abilities in case of neurodegenerative and neuropsychological disorders.
*ROS↓, As an antioxidant, allicin fights the reactive oxygen species (ROS) by downregulation of NOX (NADPH oxidizing) enzymes, it can directly interact to reduce the cellular levels of different types of ROS produced by a variety of peroxidases.
*NOX↓,
*TLR4↓, inhibition of TLR4/MyD88/NF-κB, P38 and JNK pathways.
*NF-kB↓,
*JNK↓,
*AntiAg↑, A low concentration of allicin (0.4 mM) can inhibit the platelet aggregation up to 90%, the impact is significantly higher than of similar concentration of aspirin.
*H2S↑, Allicin decomposes rapidly and undergoes a series of reactions with glutathione resulting in the production of hydrogen sulphide (H2S).
*BP↓, H2S is a gaseous signalling molecule involved in the regulation of blood pressure.
Telomerase↓, Allicin inhibits the activity of telomerase in a dose dependent manner subsequently inhibiting the proliferation in the cancer cells
*Insulin↑, Studies have shown a significant increase in the blood insulin levels after treatment with allicin
BioAv↝, optimum temperature for the activity of alliinase is 33 °C, it operates best at pH 6.5, the enzyme is sensitive to acids [42,43] (Figure 3), enteric-coated formulations of garlic supplements are therefore recommended
*GSH↑, It helps to lower the hyperglycaemic conditions and improves the glutathione and catalase biosynthesis [37,38]
*Catalase↑,

2646- AL,    Anti-Cancer Potential of Homemade Fresh Garlic Extract Is Related to Increased Endoplasmic Reticulum Stress
- in-vitro, Pca, DU145 - in-vitro, Melanoma, RPMI-8226
AntiCan↑, simple homemade ethanol-based garlic extract (GE). We show that GE inhibits growth of several different cancer cells in vitro
eff↓, These activities were lost during freeze or vacuum drying, suggesting that the main anti-cancer compounds in GE are volatile.
ChemoSen↑, We found that GE enhanced the activities of chemotherapeutics
ER Stress↑, Our data indicate that the reduced proliferation of the cancer cells treated by GE is at least partly mediated by increased endoplasmic reticulum (ER) stress.
tumCV↓, homemade GE was found to reduce the viability of the two multiple myeloma (MM) cell lines, RPMI-8226 and JJN3, as well as the prostate cancer cell line DU145 in a dose-dependent manner,
DNAdam↑, GE alone slightly increased the percentage of tail DNA (% Tail) (representing cumulative levels of abasic sites, as well as single- and double-strand DNA breaks) measured at day one, compared to untreated cells
GSH∅, We could not detect any changes in cellular GSH levels after treatments with GE
HSP70/HSPA5↓, ; however, in support of increased ER stress after GE treatment, we detected an increased pulldown of HSPA5 (BIP), a member of the Hsp70 family
UPR↑, s leading to the accumulation of unfolded proteins in the ER (also known as GRP78)
β-catenin/ZEB1↓, we also found a reduction in the β-catenin leve
ROS↑, In further support for increased ER stress induced by GE, which will lead to elevated ROS-levels and oxidative stress
HO-2↑, we found a significant increase in proteins activated by and important for regulating cellular ROS levels, e.g., OXR1, Txnl1, Hmox2, and Sirt1
SIRT1↑,
GlucoseCon∅, glucose consumption, as well as lactate secretion, were not changed.
lactateProd∅,
chemoP↑, Garlic is reported to reduce cisplatin-induced nephrotoxicity and oxidative stress

2660- AL,    Allicin: A review of its important pharmacological activities
- Review, AD, NA - Review, Var, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, It showed neuroprotective effects, exhibited anti-inflammatory properties, demonstrated anticancer activity, acted as an antioxidant, provided cardioprotection, exerted antidiabetic effects, and offered hepatoprotection.
AntiCan↑,
*antiOx↑,
*cardioP↑, This vasodilatory effect helps protect against cardiovascular diseases by reducing the risk of hypertension and atherosclerosis.
*hepatoP↑,
*BBB↑, This allows allicin to easily traverse phospholipid bilayers and the blood-brain barrier
*Half-Life↝, biological half-life of allicin is estimated to be approximately one year at 4°C. However, it should be noted that its half-life may differ when it is dissolved in different solvents, such as vegetable oil
*H2S↑, allicin undergoes metabolism in the body, leading to the release of hydrogen sulfide (H2S)
*BP↓, H2S acts as a vasodilator, meaning it relaxes and widens blood vessels, promoting blood flow and reducing blood pressure.
*neuroP↑, It acts as a neuromodulator, regulating synaptic transmission and neuronal excitability.
*cognitive↑, Studies have suggested that H2S may enhance cognitive function and protect against neurodegenerative diseases like Alzheimer's and Parkinson's by promoting neuronal survival and reducing oxidative stress.
*neuroP↑, various research studies suggest that the neuroprotective mechanisms of allicin can be attributed to its antioxidant and anti-inflammatory properties
*ROS↓,
*GutMicro↑, may contribute to the overall health of the gut microbiota.
*LDH↓, Liu et al. found that allicin treatment led to a significant decrease in the release of lactate dehydrogenase (LDH),
*ROS↓, allicin's capacity to lower the production of reactive oxygen species (ROS), decrease lipid peroxidation, and maintain the activities of antioxidant enzymes
*lipid-P↓,
*antiOx↑,
*other↑, allicin was found to enhance the expression of sphingosine kinases 2 (Sphk2), which is considered a neuroprotective mechanism in ischemic stroke
*PI3K↓, allicin downregulated the PI3K/Akt/nuclear factor-kappa B (NF-κB) pathway, inhibiting the overproduction of NO, iNOS, prostaglandin E2, cyclooxygenase-2, interleukin-6, and tumor necrosis factor-alpha induced by interleukin-1 (IL-1)
*Akt↓,
*NF-kB↓,
*NO↓,
*iNOS↓,
*PGE2↓,
*COX2↓,
*IL6↓,
*TNF-α↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
*MPO↓, Furthermore, allicin significantly decreased tumor necrosis factor-alpha (TNF-α) levels and myeloperoxidase (MPO) activity, indicating its neuroprotective effect against brain ischemia via an anti-inflammatory pathway
*eff↑, Allicin, in combination with melatonin, demonstrated a marked reduction in the expression of nuclear factor erythroid 2-related factor 2 (Nrf-2), Kelch-like ECH-associated protein 1 (Keap-1), and NF-κB genes in rats with brain damage induced by acryl
*NRF2↑, Allicin treatment decreased oxidative stress by upregulating Nrf2 protein and downregulating Keap-1 expression.
*Keap1↓,
*TBARS↓, It significantly reduced myeloperoxidase (MPO) and thiobarbituric acid reactive substances (TBARS) levels,
*creat↓, and decreased blood urea nitrogen (BUN), creatinine, LDH, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and malondialdehyde (MDA) levels.
*LDH↓,
*AST↓,
*ALAT↓,
*MDA↓,
*SOD↑, Allicin also increased the activity of superoxide dismutase (SOD) as well as the levels of glutathione S-transferase (GST) and glutathione (GSH) in the liver, kidneys, and brain
*GSH↑,
*GSTs↑,
*memory↑, Allicin has demonstrated its ability to improve learning and memory deficits caused by lead acetate injury by promoting hippocampal astrocyte differentiation.
chemoP↑, Allicin safeguards mitochondria from damage, prevents the release of cytochrome c, and decreases the expression of pro-apoptotic factors (Bax, cleaved caspase-9, cleaved caspase-3, and p53) typically activated by cisplatin
IL8↓, Allicin has been found to regulate the immune system and reduce the levels of TNF-α and IL-8.
Cyt‑c↑, In addition, allicin was reported to induce cytochrome c, increase expression of caspase 3 [86], caspase 8, 9 [82,87], caspase 12 [80] along with enhanced p38 protein expression levels [81], Fas expression levels [82].
Casp3↑,
Casp8↑,
Casp9↑,
Casp12↑,
p38↑,
Fas↑,
P53↑, Also, significantly increased p53, p21, and CHK1 expression levels decreased cyclin B after allicin treatment.
P21↑,
CHK1↓,
CycB/CCNB1↓,
GSH↓, Depletion of GSH and alterations in intracellular redox status have been found to trigger activation of the mitochondrial apoptotic pathway was the antiproliferative function of allicin
ROS↑, Hepatocellular carcinoma (HCC) cells were sensitised by allicin to the mitochondrial ROS-mediated apoptosis induced by 5-fluorouracil
TumCCA↑, According to research findings, allicin has been shown to decrease the percentage of cells in the G0/G1 and S phases [87], while causing cell cycle arrest at the G2/M phase
Hif1a↓, Allicin treatment was found to effectively reduce HIF-1α protein levels, leading to decreased expression of Bcl-2 and VEGF, and suppressing the colony formation capacity and cell migration rate of cancer cells
Bcl-2↓,
VEGF↓,
TumCMig↓,
STAT3↓, antitumor properties of allicin have been attributed to various mechanisms, including promotion of apoptosis, inhibition of STAT3 signaling
VEGFR2↓, suppression of VEGFR2 and FAK phosphorylation
p‑FAK↓,

2666- AL,    Targeting the Interplay of Autophagy and ROS for Cancer Therapy: An Updated Overview on Phytochemicals
- Review, Var, NA
Inflam↓, , anti-inflammatory, anti-cancer, and immune-modulatory activities
AntiCan↑,
ROS↑, allicin treatment led to the accumulation of ROS
MAPK↑, activation of MAPK/JNK
JNK↑,
TumAuto↑, of autophagy in non small cell lung cancer (NSCLC) cells.
other↑, autophagy at a low dose of allicin is cytoprotective
Dose↝, whereas a high dose of allicin leads to autophagic cell death.
MALAT1↓, allicin could considerably induce oxidative stress and autophagy to suppress osteosarcoma growth via inactivating the MALAT1-miR-376a-Wnt/β-catenin axis,
Wnt↓,
β-catenin/ZEB1↓,

2667- AL,    Allicin in Digestive System Cancer: From Biological Effects to Clinical Treatment
- Review, GC, NA
AntiCan↑, Allicin not only protects against tumors but also alleviates the adverse effects of anticancer treatment and enhances the chemotherapeutic response under certain conditions.
ChemoSen↑,
angioG↓, DATS works against tumors by blocking the cell cycle, inhibiting tumor cell proliferation, and inhibiting angiogenesis
chemoP↑,
*GutMicro↑, In addition to against bacteria, allicin has also been shown to modulate the composition of gut microbiota (GM) and increase the diversity of beneficial bacteria in animal models
*antiOx↑, allicin was confirmed to have strong antioxidant properties
other↝, Allicin is a reactive sulfur species (RSS) and a potent thiol-trapping reagent, rapidly reacting with glutathione (GSH) to yield S-allylmercaptoglutathione (GSSA)
GSH↓, Thus, allicin depletes the intracellular GSH pool and reacts with cysteine thiols available in proteins through S-thioallylation
Thiols↓, This reaction is the key to the biological activity of allicin, and the reversible oxidation and reduction of protein-thiols is the core of many processes in cells
*ROS↓, In a hypertrophic heart mouse model, the clearance of intracellular ROS by allicin was measured, and has been shown to reduce the production of ROS and block ROS-dependent ERK1/2, JNK1/2, AKT, NF-κB and Smad signaling, which leads to the inhibition o
*hepatoP↑, Moreover, allicin has been proven to play a hepatoprotective role against acetaminophen (APAP)-induced liver injury by reducing oxidative stress
*Inflam↓, OSCs in garlic has been shown to inhibit the tumor-mediated pro-inflammatory activity by modulating the cytokine pattern in a way that leads to an overall inhibition of NF-κB
*NF-kB↓,

3438- ALA,    The Potent Antioxidant Alpha Lipoic Acid
- Review, NA, NA - Review, AD, NA
*antiOx↑, Both of alpha lipoic acid and its reduced form have been shown to possess anti-oxidant, cardiovascular, cognitive, anti-ageing, detoxifying, anti-inflammatory, anti-cancer, and neuroprotective pharmacological properties
*cardioP↑,
*cognitive↑, Alpha lipoic acid has the ability to decrease cognitive impairment and may be a successful therapy for Alzheimer’s disease and any disease related dementias
*AntiAge↑,
*Inflam↓,
*AntiCan↑,
*neuroP↑, ALA has neuroprotective effects in experimental brain injury caused by trauma and subarachnoid hemorrhage
*IronCh↑, Also, the ability of ALA to chelate metals can produce an antioxidant effect
*ROS↑, DHLA can exert a pro-oxidant effect of donating its electrons for the reduction of iron, which can then break down peroxide to the prooxidant hydroxyl radical via the Fenton reaction [10]. So, ALA and its reduced form DHLA, can promote antioxidant pr
*Weight↓, α-lipoic acid supplementation at a dose of 300 mg/day might help to could help to promote weight loss and fat mass reduction in healthy overweight/obese women following an energy-restricted balanced diet
*Ach↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*ROS↓, also scavenges reactive oxygen species, thereby increasing the concentration levels of reduced Glutathione (GSH).
*GSH↑,
*lipid-P↓, Alpha lipoic acid can scavenge lipid peroxidation products as hydroxynonenal and acrolein.
*memory↑, learning and memory in the passive avoidance test partially through its antioxidant activity.
*NRF2↑, α-LA treatment has been shown to increase Nrf2 nuclear localization
*ChAT↑, Alpha lipoic acid increases the production of Acetylcholine (Ach) via activating choline acetyl transferase and increases glucose uptake, hence, supplying more acetyl-CoA for the production of Ach of each
*GlucoseCon↑,
*Acetyl-CoA↑,

3443- ALA,    Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention
- Review, Var, NA - Review, AD, NA
*antiOx↑, antioxidant potential and free radical scavenging activity.
*ROS↓,
*IronCh↑, Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.
*cognitive↑, α-Lipoic acid enantiomers and its reduced form have antioxidant, cognitive, cardiovascular, detoxifying, anti-aging, dietary supplement, anti-cancer, neuroprotective, antimicrobial, and anti-inflammatory properties.
*cardioP↓,
AntiCan↑,
*neuroP↑,
*Inflam↓, α-Lipoic acid can reduce inflammatory markers in patients with heart disease
*BioAv↓, bioavailability in its pure form is low (approximately 30%).
*AntiAge↑, As a dietary supplements α-lipoic acid has become a common ingredient in regular products like anti-aging supplements and multivitamin formulations
*Half-Life↓, it has a half-life (t1/2) of 30 min to 1 h.
*BioAv↝, It should be stored in a cool, dark, and dry environment, at 0 °C for short-term storage (few days to weeks) and at − 20 °C for long-term storage (few months to years).
other↝, Remarkably, neither α-lipoic acid nor dihydrolipoic acid can scavenge hydrogen peroxide, possibly the most abundant second messenger ROS, in the absence of enzymatic catalysis.
EGFR↓, α-Lipoic acid inhibits cell proliferation via the epidermal growth factor receptor (EGFR) and the protein kinase B (PKB), also known as the Akt signaling, and induces apoptosis in human breast cancer cells
Akt↓,
ROS↓, α-Lipoic acid tramps the ROS followed by arrest in the G1 phase of the cell cycle and activates p27 (kip1)-dependent cell cycle arrest via changing of the ratio of the apoptotic-related protein Bax/Bcl-2
TumCCA↑,
p27↑,
PDH↑, α-Lipoic acid drives pyruvate dehydrogenase by downregulating aerobic glycolysis and activation of apoptosis in breast cancer cells, lactate production
Glycolysis↓,
ROS↑, HT-29 human colon cancer cells; It was concluded that α-lipoic acid induces apoptosis by a pro-oxidant mechanism triggered by an escalated uptake of mitochondrial substrates in oxidizable form
*eff↑, Several studies have found that combining α-lipoic acid and omega-3 fatty acids has a synergistic effect in slowing functional and cognitive decline in Alzheimer’s disease
*memory↑, α-lipoic acid inhibits brain weight loss, downregulates oxidative tissue damage resulting in neuronal cell loss, repairs memory and motor function,
*motorD↑,
*GutMicro↑, modulates the gut microbiota without reducing the microbial diversity (

1546- Api,    Apigenin in Cancer Prevention and Therapy: A Systematic Review and Meta-Analysis of Animal Models
- Review, NA, NA
TumVol↓, Apigenin reduces tumor volume (SMD=-3.597, 95% CI: -4.502 to -2.691, p<0.001)
TumW↓, tumor-weight (SMD=-2.213, 95% CI: -2.897 to -1.529, p<0.001)
AntiCan↑, tumor number (SMD=-1.081, 95% CI: -1.599 to -0.563, p<0.001) and tumor load (SMD=-1.556, 95% CI: -2.336 to -0.776, p<0.001).
Apoptosis↑, exerts anti-tumor effects mainly by inducing apoptosis/cell-cycle arrest
TumCCA↑,

1561- Api,    Apigenin Reactivates Nrf2 Anti-oxidative Stress Signaling in Mouse Skin Epidermal JB6 P + Cells Through Epigenetics Modifications
- in-vivo, Nor, JB6
*NRF2↑, API enhanced the nuclear translocation of Nrf2
*DNMT1↓, API reduced the expression of the DNMT1, DNMT3a, and DNMT3b epigenetic proteins as well as the expression of some HDACs (1–8).
*DNMT3A↓,
*HDAC↓,
*AntiCan↑, results may provide new therapeutic insights into the prevention of skin cancer by dietary phytochemicals.

2636- Api,    Apigenin unveiled: an encyclopedic review of its preclinical and clinical insights
- Review, NA, NA
*AntiCan↑, clinical studies are beginning to affirm apigenin's therapeutic benefits, showing positive effects in treating cancer, cardiovascular diseases, diabetes, neurodegenerative disorders, and inflammatory conditions.
*cardioP↑, The findings suggest that apigenin could serve as an effective therapeutic agent to reduce cardiotoxicity caused by Doxorubicin
*neuroP↑,
*Inflam↓,
*antiOx↑, apigenin (5,7,4′-trihydroxyflavone) is a flavonoid that chelates redox-active metals and has antioxidant properties
*hepatoP↑, Overall, the results indicate that apigenin alleviated liver injury by reducing inflammation and oxidative stress via suppression of the non-canonical NF-κB pathway
ChemoSen↑, Apigenin increases the cytotoxicity of sorafenib

2639- Api,    Plant flavone apigenin: An emerging anticancer agent
- Review, Var, NA
*antiOx↑, Apigenin (4′, 5, 7-trihydroxyflavone), a major plant flavone, possessing antioxidant, anti-inflammatory, and anticancer properties
*Inflam↓,
AntiCan↑,
ChemoSen↑, Studies demonstrate that apigenin retain potent therapeutic properties alone and/or increases the efficacy of several chemotherapeutic drugs in combination on a variety of human cancers.
BioEnh↑, Apigenin’s anticancer effects could also be due to its differential effects in causing minimal toxicity to normal cells with delayed plasma clearance and slow decomposition in liver increasing the systemic bioavailability in pharmacokinetic studies.
chemoPv↑, apigenin highlighting its potential activity as a chemopreventive and therapeutic agent.
IL6↓, In taxol-resistant ovarian cancer cells, apigenin caused down regulation of TAM family of tyrosine kinase receptors and also caused inhibition of IL-6/STAT3 axis, thereby attenuating proliferation.
STAT3↓,
NF-kB↓, apigenin treatment effectively inhibited NF-κB activation, scavenged free radicals, and stimulated MUC-2 secretion
IL8↓, interleukin (IL)-6, and IL-8
eff↝, The anti-proliferative effects of apigenin was significantly higher in breast cancer cells over-expressing HER2/neu but was much less efficacious in restricting the growth of cell lines expressing HER2/neu at basal levels
Akt↓, Apigenin interferes in the cell survival pathway by inhibiting Akt function by directly blocking PI3K activity
PI3K↓,
HER2/EBBR2↓, apigenin administration led to the depletion of HER2/neu protein in vivo
cycD1/CCND1↓, Apigenin treatment in breast cancer cells also results in decreased expression of cyclin D1, D3, and cdk4 and increased quantities of p27 protein
CycD3↓,
p27↑,
FOXO3↑, In triple-negative breast cancer cells, apigenin induces apoptosis by inhibiting the PI3K/Akt pathway thereby increasing FOXO3a expression
STAT3↓, In addition, apigenin also down-regulated STAT3 target genes MMP-2, MMP-9, VEGF and Twist1, which are involved in cell migration and invasion of breast cancer cells [
MMP2↓,
MMP9↓,
VEGF↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
Twist↓,
MMP↓, Apigenin treatment of HGC-27 and SGC-7901 gastric cancer cells resulted in the inhibition of proliferation followed by mitochondrial depolarization resulting in apoptosis
ROS↑, Further studies revealed apigenin-induced apoptosis in hepatoma tumor cells by utilizing ROS generated through the activation of the NADPH oxidase
NADPH↑,
NRF2↓, Apigenin significantly sensitized doxorubicin-resistant BEL-7402 (BEL-7402/ADM) cells to doxorubicin (ADM) and increased the intracellular concentration of ADM by reducing Nrf2-
SOD↓, In human cervical epithelial carcinoma HeLa cells combination of apigenin and paclitaxel significantly increased inhibition of cell proliferation, suppressing the activity of SOD, inducing ROS accumulation leading to apoptosis by activation of caspas
COX2↓, melanoma skin cancer model where apigenin inhibited COX-2 that promotes proliferation and tumorigenesis
p38↑, Additionally, it was shown that apigenin treatment in a late phase involves the activation of p38 and PKCδ to modulate Hsp27, thus leading to apoptosis
Telomerase↓, apigenin inhibits cell growth and diminishes telomerase activity in human-derived leukemia cells
HDAC↓, demonstrated the role of apigenin as a histone deacetylase inhibitor. As such, apigenin acts on HDAC1 and HDAC3
HDAC1↓,
HDAC3↓,
Hif1a↓, Apigenin acts on the HIF-1 binding site, which decreases HIF-1α, but not the HIF-1β subunit, thereby inhibiting VEGF.
angioG↓, Moreover, apigenin was found to inhibit angiogenesis, as suggested by decreased HIF-1α and VEGF expression in cancer cells
uPA↓, Furthermore, apigenin intake resulted in marked inhibition of p-Akt, p-ERK1/2, VEGF, uPA, MMP-2 and MMP-9, corresponding with tumor growth and metastasis inhibition in TRAMP mice
Ca+2↑, Neuroblastoma SH-SY5Y cells treated with apigenin led to induction of apoptosis, accompanied by higher levels of intracellular free [Ca(2+)] and shift in Bax:Bcl-2 ratio in favor of apoptosis, cytochrome c release, followed by activation casp-9, 12
Bax:Bcl2↑,
Cyt‑c↑,
Casp9↑,
Casp12↑,
Casp3↑, Apigenin also augmented caspase-3 activity and PARP cleavage
cl‑PARP↑,
E-cadherin↑, Apigenin treatment resulted in higher levels of E-cadherin and reduced levels of nuclear β-catenin, c-Myc, and cyclin D1 in the prostates of TRAMP mice.
β-catenin/ZEB1↓,
cMyc↓,
CDK4↓, apigenin exposure led to decreased levels of cell cycle regulatory proteins including cyclin D1, D2 and E and their regulatory partners CDK2, 4, and 6
CDK2↓,
CDK6↓,
IGF-1↓, A reduction in the IGF-1 and increase in IGFBP-3 levels in the serum and the dorsolateral prostate was observed in apigenin-treated mice.
CK2↓, benefits of apigenin as a CK2 inhibitor in the treatment of human cervical cancer by targeting cancer stem cells
CSCs↓,
FAK↓, Apigenin inhibited the tobacco-derived carcinogen-mediated cell proliferation and migration involving the β-AR and its downstream signals FAK and ERK activation
Gli↓, Apigenin inhibited the self-renewal capacity of SKOV3 sphere-forming cells (SFC) by downregulating Gli1 regulated by CK2α
GLUT1↓, Apigenin induces apoptosis and slows cell growth through metabolic and oxidative stress as a consequence of the down-regulation of glucose transporter 1 (GLUT1).

3382- ART/DHA,    Repurposing Artemisinin and its Derivatives as Anticancer Drugs: A Chance or Challenge?
- Review, Var, NA
AntiCan↑, antimalarial drug, artemisinin that has shown anticancer activities in vitro and in vivo.
toxicity↑, safety of artemisinins in long-term cancer therapy requires further investigation.
Ferroptosis↑, Artemisinins acts against cancer cells via various pathways such as inducing apoptosis (Zhu et al., 2014; Zuo et al., 2014) and ferroptosis via the generation of reactive oxygen species (ROS) (Zhu et al., 2021) and causing cell cycle arrest
ROS↑,
TumCCA↑,
BioAv↝, absolute bioavailability was estimated to be 21.6%. ART has good solubility and is not lipophilic
eff↝, ART would not distribute well to the tissues and might be more effective in treating cancers such as leukemia, hepatocellular carcinoma (HCC), or renal cell carcinoma because the liver and kidney are highly perfused organs.
Half-Life↓, Pharmacokinetic studies showed a relatively short t1/2 of artemisinins. For ART, t1/2 was 0.41 h
Ferritin↓, Figure 3
GPx4↓,
NADPH↓,
GSH↓,
BAX↑,
Cyt‑c↑,
cl‑Casp3↑,
VEGF↓, angiogenesis
IL8↓,
COX2↓,
MMP9↓,
E-cadherin↑,
MMP2↓,
NF-kB↓,
p16↑, cell cycle arrest
CDK4↓,
cycD1/CCND1↓,
p62↓, autophagy
LC3II↑,
EMT↓, suppressing EMT and CSCs
CSCs↓,
Wnt↓, Depress Wnt/β-catenin signaling pathway
β-catenin/ZEB1↓,
uPA↓, Inhibit u-PA activity, protein and mRNA expression
TumAuto↑, Emerging evidence suggests that autophagy induction is one of the molecular mechanisms underlying anticancer activity of artemisinins
angioG↓, Inhibition of Angiogenesis
ChemoSen↑, Many studies also reported that the use of artemisinins sensitized cancer cells to conventional chemotherapy and exerted a synergistic effect on apoptosis, inhibition of cell growth, and a reduction of cell viability, leading to a lower IC50 value

5382- ART/DHA,    A phase I study of intravenous artesunate in patients with advanced solid tumor malignancies
- Trial, Var, NA
AntiCan↑, The artemisinin class of anti-malarial drugs has shown significant anti-cancer activity in pre-clinical models.
Dose↝, maximum tolerated dose (MTD) . maximum tolerated dose (MTD) a
Dose↝, MTD of intravenous artesunate is 18 mg/kg

5378- ART/DHA,    Natural Agents Modulating Ferroptosis in Cancer: Molecular Pathways and Therapeutic Perspectives
- Review, Var, NA
Ferroptosis↑, Artemisinin increases ferroptosis risk in cancer cells by increasing cellular free iron and lipid peroxidation, causing increased membrane permeability and decreased integrity [59]
Iron↑,
lipid-P↑,
MOMP↑,
AntiCan↑, Artemisinin has anticancer and antimalarial properties by upregulating NCOA4 and DMT1 levels, raising ferrous ion levels, and causing ferroptosis by downregulating GSH and GPX4 levels [30, 59, 75].
NCOA4↑,
GSH↓,
GPx4↓,
ROS↑, Artemisinin and its derivatives regulate 20 iron metabolism genes, thereby causing the formation of ROS [76]
ChemoSen↑, Artesunate, when combined with sorafenib, can enhance the susceptibility of hepatocellular carcinoma cells to cisplatin resistance through ferroptosis inhibition [77].
ER Stress↑, artemisinin, specifically ferroptosis, by controlling iron metabolism, producing ROS, and triggering ER‐stress.
DNAdam↑, primary antineoplastic mechanisms of artemisinin are ferroptosis, DNA damage, tumour angiogenesis suppression and cell cycle inhibition [78]
angioG↓,
TumCCA↑,
eff↓, while NAC and ferrostatin‐1 partially reverse these effects [82]

5377- ART/DHA,    Dihydroartemisinin-induced ferroptosis in acute myeloid leukemia: links to iron metabolism and metallothionein
- in-vitro, AML, NA
AntiCan↑, Artemisinin is an anti-malarial drug that has shown anticancer properties
Ferroptosis↑, Recently, ferroptosis was reported to be induced by dihydroartemisinin (DHA) and linked to iron increase.
Iron↑, We found that treatment of DHA induces early ferroptosis by promoting ferritinophagy and subsequent iron increase.
Mets↑, Furthermore, our study demonstrated that DHA activated zinc metabolism signaling, especially the upregulation of metallothionein (MT).
eff↑, Supportingly, we showed that inhibition MT2A and MT1M isoforms enhanced DHA-induced ferroptosis.
GSH↝, Finally, we demonstrated that DHA-induced ferroptosis alters glutathione pool, which is highly dependent on MTs-driven antioxidant response.
eff↑, DHA cooperates with FAC to increase the intracellular iron pool. ferric citrate iron (FAC)
other↓, Under oxidative stress, MT can release Zn2+ (apo-MT) to form thiol groups and participates in GSSG/ GSH reduction.
eff↑, Our current findings also suggest that MT chemical inhibition can cooperate with DHA in primary AML cells in patients.
other↓, Subsequent MT inhibition may sensitize leukemic cells to lipid peroxidation in vitro by impairing GSH regeneration.

5395- Ash,    Withaferin A Targets Heat Shock Protein 90 in Pancreatic Cancer Cells
- vitro+vivo, PC, PANC1 - in-vitro, PC, MIA PaCa-2
TumCP↓, Withaferin A exhibited potent antiproliferative activity against pancreatic cancer cells in vitro
HSP90↓, WA inhibited Hsp90 chaperone activity to induce degradation of Hsp90 client proteins (Akt, Cdk4 and glucocorticoid receptor)
Akt↓,
CDK4↓,
TumCG↓, WA (3, 6 mg/kg) inhibited tumor growth in pancreatic Panc-1 xenografts by 30% and 58%, respectively.
Apoptosis↑, Withaferin A induces apoptosis in pancreatic cancer cells
AntiCan↑, Withaferin A exhibits anticancer activity in pancreatic cancer xenografts

5384- AsP,  MEL,    Synergistic Anticancer Effect of Melatonin and Ascorbyl Palmitate Nanoformulation: A Promising Combination for Cancer Therapy
- in-vivo, Var, NA
AntiCan↑, assess the anticancer effect of melatonin (MEL) and ascorbyl palmitate-loaded pluronic nanoparticles (APnp) combination on Ehrlich ascites carcinoma (EAC)-bearing mice.
TumCG↓, MEL alone showed a decrease in tumor growth by 48%, while in the case of using MEL combined with APnp, it displayed inhibition of tumor growth by 62%
Apoptosis↑, It also induced apoptosis and DNA damage.
DNAdam↑,
TumCCA↑, Besides, mediated cell cycle arrest.
IL6↓, IL-6/STAT3 pathway was inactivated to a greater extent after our combination treatment.
STAT3↓,
TumCP↓, antiproliferative effect of MEL and APnp via decreased expression of Ki-67
Ki-67↓,
TumCI↓, Our combination of MEL and APnp was able to inhibit cancer cell invasion and metastasis by decreasing the protein expression of MMP-9.
TumMeta↓,
MMP9↓,
eff↑, The synergy score was 21.06 ( > 10 indicates synergistic effect)
*Catalase↑, Administration of MEL alone or MEL+ APnp treated mice showed a significant and highly significant increase, respectively (P<0.05, P<0.01) in the antioxidant enzyme activities of CAT and SOD, and GSH.
*SOD↑,
*GSH↑,
*MDA↓, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control group.
*NO↓,
*antiOx↑, Figure 2 demonstrated a highly significant and extremely significant reduction, respectively (P<0.01, P<0.001) in the MDA and NO levels compared to the EAC control group.
*hepatoP↑, combined MEL and APnp- treated animals displayed a noteworthy amelioration for all examined organs when compared to the control EAC inoculated group, Figure 3.
*RenoP↑,

4814- ASTX,    Chemopreventive and therapeutic efficacy of astaxanthin against cancer: A comprehensive review
- Review, Var, NA
Apoptosis↑, Astaxanthin causes apoptosis in several in vitro studies, including both oral and liver cancer cells
EMT↓, AXT inhibits the EMT pathway in colon cancer cells and can reduce breast cancer cells' proliferation and growth
AntiCan↑, Astaxanthin can address human health problems, including cancer, cardiovascular, and neurodegenerative diseases.
*cardioP↑,
*neuroP↑,
TumCG↓, 100 mg/kg Astaxanthin strongly inhibited tumor growth relative to the TC group, with an inhibitory rate of 41.7%.
*antiOx↑, .ASX is often referred to as the "super antioxidant" since it has the strongest antioxidant activity of current carotenoids.
*Bacteria↓, Studies have demonstrated antioxidant and antimicrobial, immunomodulatory, hepatoprotective, anticancer, and antidiabetic effects of ASX.
*Imm↑,
*hepatoP↑,
*AntiDiabetic↑,
ROS↓, Astaxanthin and carbendazim function in conjunction to inhibit cell proliferation while reducing ROS production in breast cancer cells.
*chemoPv↑, Chemopreventive and therapeutic efficacy of astaxanthin against cancer

4804- ASTX,    Astaxanthin in cancer therapy and prevention (Review)
- Review, Var, NA - Review, AD, NA
*antiOx↑, gained significant attention for its potent antioxidant, anti-inflammatory and anti-proliferative properties.
*Inflam↓,
ChemoSen⇅, In some instances, it reduces the cytotoxicity of cisplatin, particularly with cisplatin on the SKBR3 breast cancer cell line, indicating a potential protective effect. In certain cases, AXT enhances the cytotoxic effect of the chemotherapy drugs
chemoP↑, The present review detailed both in vitro and in vivo studies highlighting the effectiveness of AXT in sensitizing cancer cells to chemotherapy, thereby enhancing therapeutic outcomes and potentially reducing treatment-related side effects.
BioAv↑, incorporation of AXT in nanoparticle-based delivery systems has further improved its bioavailability
TumCP↑, AXT exhibits hormetic effects on U251-MG, T98G and CRT-MG cell lines, where low doses stimulate cell proliferation
ROS⇅, while higher doses induce apoptosis by triggering a dose-dependent oxidative stress response, significantly increasing reactive oxygen species (ROS) levels and promoting apoptosis
Apoptosis↑,
PI3K↑, AXT activates the PI3K/Akt/GSK3β pathway, leading to the upregulation of nuclear factor erythroid 2-related factor 2 (Nrf2), a transcription factor, in SH-SY5Y cells under oxygen and glucose deprivation conditions
Akt↑,
GSK‐3β↑,
NRF2↑,
AntiCan↑, antioxidant, AXT has the potential to act as both an anticancer drug and a neuroprotectant.
*neuroP↑, AXT protects against oxidative stress, which causes mitochondrial dysfunction and apoptosis, thereby reducing the detrimental effects associated with neurodegenerative diseases such as Alzheimer's, Parkinson's
eff↑, The synergistic cytotoxic effect of AXT with melatonin showed enhanced efficacy in the T47D cell line compared with the MDA-MB-231 line
AntiTum↑, AXT effectively reduced tumor size and the number of cancer cells in mice, supporting its potential anti-tumor activity.

4807- ASTX,    An overview of the anticancer activity of astaxanthin and the associated cellular and molecular mechanisms
- Review, Var, NA
*antiOx↑, Reports indicate that ASX’s antioxidant efficacy surpasses that of vitamin C, vitamin E, coenzyme Q10, and alpha-lipoic acid.
*neuroP↑, Astaxanthin is a powerful antioxidant compound that supports heart, skin, and eye health, helps manage diabetes, and offers brain-protective benefits.
AntiCan↑, Astaxanthin shows promise as an anticancer agent by limiting tumor growth, inducing cancer cell death, and reducing the spread of malignant cells.
TumCG↓,
TumCD↑,
TumCMig↓,
ChemoSen↑, Astaxanthin enhances the effects of chemotherapy, reduces its side effects, and helps overcome drug resistance.
chemoP↑,
*BioAv↓, Astaxanthin has limited absorption in the body, but using nanocarriers like nanoparticles and nano-emulsions can greatly enhance its bioavailability and therapeutic potential.
TumCP↓, ASX inhibits tumor formation, primarily by hindering cell proliferation, inducing cell cycle arrest, and promoting apoptosis.
TumCCA↑,
Apoptosis↑,
BioAv↑, Nanotechnology: a solution for improving astaxanthin bioavailability

5427- ASTX,    Astaxanthin and Cancer Chemoprevention
- Review, Var, NA
chemoP↑, evidence for anticarcinogenic behavior of selected carotenoids, with an emphasis on the chemopreventive activities of astaxanthin.
AntiCan↑, Human epidemiological studies have revealed a protective effect of vegetable and fruit consumption for cancers of the stomach, esophagus, lung, oral cavity and pharynx, bladder, endometrium, pancreas, colon and rectum, breast, cervix, ovary and prost
chemoPv↑, the chemopreventive effects of canthaxanthin
Risk↓, Salmon, the principal dietary source of astaxanthin, is an important component of the traditional diets of Eskimos and certain coastal tribes in North America; these groups have shown unusually low prevalence of cancer.
lipid-P↓, Dietary astaxanthin also reduced metastatic nodules and lipid peroxidation in the livers of rats treated with restraint stress.
Pain↓, The results revealed that astaxanthin significantly relieved pain and improved performance in patients with RA
BioAv↑, the results demonstrated an enhancement of astaxanthin bioavailability in humans when incorporated into lipid-based formulations.
Dose↝, relevant dietary dosages of astaxanthin (4-12 mg daily is typically recommended by supplement manufacturers),

5419- ASTX,    Astaxanthin and other Nutrients from Haematococcus pluvialis—Multifunctional Applications
- Review, Nor, NA
*antiOx↑, extraction of astaxanthin and analysis of its antioxidant, anti-inflammatory, anti–diabetic and anticancer activities.
*Inflam↓,
*AntiDiabetic↓,
AntiCan↑,
*lipid-P↓, astaxanthin is more effective than β-carotene in the prevention of lipid peroxidation.
TumCP↓, Studies have reported that astaxanthin not only inhibits the proliferation of colon cancer cells but can also cause their apoptosis
Apoptosis↑,
TumCCA↑, Astaxanthin was included in the extract and was responsible for stopping the progression of the cell cycle and promoting the apoptosis [95].
*SOD↑, Astaxanthin also increased SOD activity and decreased PG-E2, LT-B4, NO, IL-8 and IFN- γ production [103,104,105].
*PGE2↓,
*NO↓,
*IL8↓,
*IFN-γ↓,
*cardioP↑, Astaxanthin has a cardiovascular protective effect in animals, but there is a lack of research supporting the therapeutic benefit of astaxanthin in atherosclerotic cardiovascular disease in humans.
*NF-kB↓, Oral supplementation with astaxanthin in rats after surgery decreased the expression of NF-KB and TNF-α,
*TNF-α↓,
*BioAv↑, Satisfactory astaxanthin bioavailability results were obtained with a daily astaxanthin dose of 40 mg/day.

5424- ASTX,    Astaxanthin exerts an adjunctive anti-cancer effect through the modulation of gut microbiota and mucosal immunity
- in-vivo, Nor, NA
*GutMicro↑, Astaxanthin synergistically enhances the anticancer effects of sorafenib by modulating intestinal flora.
AntiCan↑,
eff↑, Astaxanthin significantly promotes the proliferation of Akkermansia, a microorganism with enhanced anti-tumor immune effects.
AntiTum↑, Therefore, it strengthens the body's anti-tumor immune response and synergistically boosts the therapeutic efficacy of drugs.
ChemoSen↑,


Showing Research Papers: 1 to 50 of 254
Page 1 of 6 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 254

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↓, 1,   antiOx↑, 1,   Ferroptosis↑, 4,   GPx4↓, 3,   GSH↓, 7,   GSH↝, 1,   GSH∅, 1,   HO-2↑, 1,   Iron↑, 2,   c-Iron↑, 1,   lipid-P↓, 1,   lipid-P↑, 3,   Mets↑, 1,   NRF2↓, 1,   NRF2↑, 2,   ROS↓, 3,   ROS↑, 22,   ROS⇅, 1,   SOD↓, 1,   Thiols↓, 2,   TrxR↓, 1,  

Metal & Cofactor Biology ⓘ

Ferritin↓, 1,   NCOA4↑, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 1,   ETC↓, 1,   MMP↓, 5,   MMP↑, 1,   MPT↑, 1,   mtDam↑, 1,   OCR↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACSL4↑, 1,   cMyc↓, 1,   GlucoseCon∅, 1,   Glycolysis↓, 1,   H2S↑, 1,   HK2↓, 1,   lactateProd∅, 1,   LDH↓, 1,   LDHA↓, 1,   NADPH↓, 1,   NADPH↑, 1,   PDH↑, 2,   SIRT1↑, 1,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 6,   Akt↑, 1,   Apoptosis↑, 19,   BAX↑, 6,   Bax:Bcl2↑, 1,   Bcl-2↓, 4,   Casp↑, 3,   Casp12↑, 2,   Casp3↑, 4,   cl‑Casp3↑, 2,   Casp8↑, 2,   Casp9↑, 2,   CK2↓, 1,   Cyt‑c↑, 6,   Fas↑, 2,   Ferroptosis↑, 4,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   MOMP↑, 1,   necrosis↑, 1,   p27↑, 4,   p38↑, 2,   survivin↓, 1,   Telomerase↓, 2,   TumCD↑, 1,  

Kinase & Signal Transduction ⓘ

AMPKα↑, 1,   HER2/EBBR2↓, 1,  

Transcription & Epigenetics ⓘ

other↓, 2,   other↑, 3,   other↝, 3,   PhotoS↑, 1,   tumCV↓, 7,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 3,   HSP70/HSPA5↓, 1,   HSP90↓, 1,   UPR↑, 2,  

Autophagy & Lysosomes ⓘ

LC3II↑, 1,   p62↓, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

CHK1↓, 1,   DNAdam↑, 10,   p16↑, 1,   P53↑, 2,   p‑P53↑, 1,   p‑PARP↑, 1,   cl‑PARP↑, 3,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 4,   CycB/CCNB1↓, 1,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 5,   CycD3↓, 1,   cycE/CCNE↓, 1,   P21↑, 4,   TumCCA↑, 16,  

Proliferation, Differentiation & Cell State ⓘ

CSCs↓, 4,   EMT↓, 3,   FOXO3↑, 1,   Gli↓, 1,   GSK‐3β↓, 1,   GSK‐3β↑, 1,   HDAC↓, 1,   HDAC1↓, 1,   HDAC3↓, 1,   IGF-1↓, 1,   mTOR↓, 2,   NOTCH1↓, 1,   PI3K↓, 4,   PI3K↑, 1,   PTEN↑, 1,   STAT3↓, 4,   TumCG↓, 6,   Wnt↓, 3,  

Migration ⓘ

Ca+2↑, 2,   E-cadherin↑, 2,   FAK↓, 1,   p‑FAK↓, 1,   Ki-67↓, 1,   MALAT1↓, 1,   MMP2↓, 2,   MMP9↓, 3,   TGF-β↓, 1,   TumCI↓, 1,   TumCMig↓, 3,   TumCP↓, 6,   TumCP↑, 1,   TumMeta↓, 1,   Twist↓, 1,   uPA↓, 2,   Vim↓, 1,   β-catenin/ZEB1↓, 5,  

Angiogenesis & Vasculature ⓘ

angioG↓, 5,   EGFR↓, 2,   EPR↑, 3,   HIF-1↓, 1,   Hif1a↓, 4,   VEGF↓, 3,   VEGFR2↓, 1,  

Barriers & Transport ⓘ

CellMemb↑, 1,   GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CXCR4↓, 1,   IL12↑, 1,   IL2↑, 1,   IL6↓, 2,   IL8↓, 3,   Imm↑, 1,   Inflam↓, 1,   NF-kB↓, 3,   NF-kB↑, 1,   NK cell↑, 1,   PD-L1↓, 1,   TNF-α↑, 1,  

Cellular Microenvironment ⓘ

pH↝, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 2,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 1,   BioAv↑, 4,   BioAv↝, 2,   BioEnh↑, 1,   ChemoSen↑, 14,   ChemoSen⇅, 1,   Dose↝, 5,   eff↓, 3,   eff↑, 16,   eff↝, 2,   Half-Life↓, 1,   MDR1↓, 1,   RadioS↑, 2,   selectivity↑, 10,  

Clinical Biomarkers ⓘ

EGFR↓, 2,   Ferritin↓, 1,   HER2/EBBR2↓, 1,   IL6↓, 2,   Ki-67↓, 1,   LDH↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 47,   AntiTum↑, 2,   chemoP↑, 7,   chemoPv↑, 2,   cognitive↑, 1,   Pain↓, 1,   QoL↑, 1,   Risk↓, 1,   toxicity↑, 1,   toxicity↝, 1,   TumVol↓, 2,   TumW↓, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 2,  
Total Targets: 197

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 15,   Catalase↑, 2,   GSH↑, 5,   GSTs↑, 1,   Keap1↓, 1,   lipid-P↓, 3,   MDA↓, 2,   MPO↓, 1,   NRF2↑, 4,   ROS↓, 6,   ROS↑, 1,   SOD↑, 3,   TBARS↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 2,  

Mitochondria & Bioenergetics ⓘ

Insulin↑, 1,  

Core Metabolism/Glycolysis ⓘ

Acetyl-CoA↑, 1,   ALAT↓, 1,   GlucoseCon↑, 1,   H2S↑, 2,   LDH↓, 2,   LDL↓, 1,  

Cell Death ⓘ

Akt↓, 1,   iNOS↓, 1,   JNK↓, 1,   JNK↑, 1,  

Transcription & Epigenetics ⓘ

Ach↑, 1,   other↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   cl‑eIF2α↑, 1,   GRP78/BiP↑, 1,   p‑PERK↑, 1,  

DNA Damage & Repair ⓘ

DNMT1↓, 1,   DNMT3A↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

HDAC↓, 1,   PI3K↓, 1,  

Migration ⓘ

AntiAg↑, 1,  

Angiogenesis & Vasculature ⓘ

NO↓, 3,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   IFN-γ↓, 1,   IL6↓, 1,   IL8↓, 1,   Imm↑, 1,   Inflam↓, 9,   NF-kB↓, 4,   PGE2↓, 2,   TLR4↓, 1,   TNF-α↓, 2,  

Cellular Microenvironment ⓘ

NOX↓, 1,  

Synaptic & Neurotransmission ⓘ

ChAT↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,   BioAv↝, 1,   eff↑, 2,   Half-Life↓, 1,   Half-Life↝, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,   BMD↑, 1,   BP↓, 3,   creat↓, 1,   GutMicro↑, 5,   IL6↓, 1,   LDH↓, 2,  

Functional Outcomes ⓘ

AntiAge↑, 2,   AntiCan↑, 4,   AntiDiabetic↓, 1,   AntiDiabetic↑, 3,   cardioP↓, 1,   cardioP↑, 7,   chemoP↑, 1,   chemoPv↑, 1,   cognitive↑, 3,   hepatoP↑, 6,   memory↑, 3,   motorD↑, 1,   neuroP↑, 9,   RenoP↑, 1,   toxicity↓, 1,   toxicity↝, 1,   Weight↓, 2,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

AntiViral↑, 1,   Bacteria↓, 5,  
Total Targets: 84

Scientific Paper Hit Count for: AntiCan, Anticancer Effect
18 Silver-NanoParticles
12 Lycopene
10 Thymoquinone
10 Selenium NanoParticles
8 Magnolol
7 Allicin (mainly Garlic)
7 Quercetin
7 Sulforaphane (mainly Broccoli)
6 Astaxanthin
6 Capsaicin
6 Curcumin
6 Gambogic Acid
6 Phenethyl isothiocyanate
5 Artemisinin
5 Vitamin C (Ascorbic Acid)
4 chitosan
4 Apigenin (mainly Parsley)
4 Baicalein
4 Boron
4 Carvacrol
4 Chlorogenic acid
4 Honokiol
4 Selenium
4 Selenite (Sodium)
3 Coenzyme Q10
3 Melatonin
3 Aloe anthraquinones
3 beta-glucans
3 Biochanin A
3 Resveratrol
3 Spermidine
3 Ellagic acid
3 Naringin
3 Propolis -bee glue
3 Pterostilbene
3 salinomycin
3 Silymarin (Milk Thistle) silibinin
3 Vitamin D3
3 Vitamin K2
2 3-bromopyruvate
2 doxorubicin
2 Alpha-Lipoic-Acid
2 Baicalin
2 Boswellia (frankincense)
2 Butyrate
2 Caffeic Acid Phenethyl Ester (CAPE)
2 Thymol-Thymus vulgaris
2 Chlorophyllin
2 Camptothecin
2 Hydroxycinnamic-acid
2 Dichloroacetate
2 Ferulic acid
2 HydroxyTyrosol
2 Magnetic Fields
2 Piperine
2 Rosmarinic acid
2 Shikonin
2 Ursolic acid
2 VitK3,menadione
1 5-fluorouracil
1 Auranofin
1 Astragalus
1 Citric Acid
1 Ashwagandha(Withaferin A)
1 Ascorbyl Palmitate
1 Berberine
1 Betulinic acid
1 Bromelain
1 borneol
1 Bruteridin(bergamot juice)
1 Vitamin B3,Niacin
1 Caffeic acid
1 Caffeine
1 urea
1 Celastrol
1 Chrysin
1 irinotecan
1 Calorie Restriction Mimetics
1 Aspirin -acetylsalicylic acid
1 diet FMD Fasting Mimicking Diet
1 diet Methionine-Restricted Diet
1 diet Plant based
1 EGCG (Epigallocatechin Gallate)
1 Electrical Pulses
1 Gallic acid
1 γ-linolenic acid (Borage Oil)
1 alpha Linolenic acid
1 Hydrogen Gas
1 Lecithin
1 Luteolin
1 Methylene blue
1 Photodynamic Therapy
1 mebendazole
1 Metformin
1 Magnetic Field Rotating
1 Bicarbonate(Sodium)
1 Oleocanthal
1 Piperlongumine
1 Psoralidin
1 Parthenolide
1 Salvia officinalis
1 Radiotherapy/Radiation
1 Date Fruit Extract
1 Calcium
1 Aflavin-3,3′-digallate
1 Urolithin
1 Magnesium
1 Zerumbone
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:813  State#:%  Dir#:2
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