tumCV Cancer Research Results

tumCV, Cell Viability: Click to Expand ⟱
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5259- 3BP,    Advanced cancers: eradication in all cases using 3-bromopyruvate therapy to deplete ATP
- in-vivo, HCC, NA
ATP↓, Advanced cancers (2-3cm) developed and were treated with the alkylating agent 3-bromopyruvate, a lactate/pyruvate analog shown here to selectively deplete ATP and induce cell death.
TumCD↑,
toxicity↓, In all 19 treated animals advanced cancers were eradicated without apparent toxicity or recurrence.
eff↑, These findings attest to the feasibility of completely destroying advanced, highly glycolytic cancers.
tumCV↓, The chemical agent 3-BrPA depletes ATP stores and inhibits HCC cell viability
Dose↝, administered eight treatments on successive days with 1 ml of 2 mM 3-BrPA, also in 1· PBS, pH 7.5. Injection of 3-BrPA was into the tumor.

5236- AgNPs,    Adaptive regulations of Nrf2 alleviates silver nanoparticles-induced oxidative stress-related liver cells injury
- in-vitro, Liver, HepG2 - in-vitro, Nor, L02
tumCV↓, AgNPs induced a concentration-dependent decline in HepG2 and L02 cells viability.
ROS↑, • AgNPs induced ROS increase and apoptosis in HepG2 and L02 cells.
*ROS↑,
DNAdam↑, AgNPs induced DNA damage, autophagy and cell cycle arrest in HepG2 and L02 cells.
*DNAdam↑,
eff↓, N-acetylcysteine (NAC)alleviated AgNPs-induced cytotoxicity in HepG2 and L02 cells.
selectivity↑, Interestingly, HepG2 cells were more sensitive to AgNPs than L02 cells, and this may be related to the different ROS generation and responses to AgNPs by cancer cells and normal cells.

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.

4397- AgNPs,    Synthesis and Characterization of Silver Nanoparticles from Rhizophora apiculata and Studies on Their Wound Healing, Antioxidant, Anti-Inflammatory, and Cytotoxic Activity
- NA, Wounds, NA
selectivity↑, The cytotoxicity cell viability assay revealed that the AgNPs were less toxic (IC50 105.5 µg/mL) compared to the R. apiculata extract (IC50 47.47 µg/mL) against the non-cancerous fibroblast L929 cell line.
tumCV↓, AgNPs showed considerable cytotoxic effect, and the percentage of cell viability against skin cancer, lung cancer, and oral cancer cell lines was 31.84%, 56.09% and 22.59%, respectively.
antiOx↑, AgNPs exhibited potential antioxidant, anti-inflammatory, wound healing, and cytotoxic properties
Inflam↓,

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.

4388- AgNPs,    Differential Cytotoxic Potential of Silver Nanoparticles in Human Ovarian Cancer Cells and Ovarian Cancer Stem Cells
- in-vitro, Cerv, NA
tumCV↓, the numbers of A2780 (bulk cells) and ALDH+/CD133+ colonies were significantly reduced
CSCs↓,
selectivity↑, induced apoptosis in pancreatic CSCs and cancer cell lines, but had no effect on human normal pancreatic epithelial cells
Apoptosis↑,
ROS↑, figure 5, AgNPs induces apoptosis by oxidative stress
LDH↓, figure 5 (leakage outside the cell increases)
Casp3↑, AgNPs treated cells shows up-regulation of caspase-3, bax, bak, and c-myc, genes
BAX↑,
Bak↑,
cMyc↑,
MMP↓, and loss of mitochondrial membrane potential.

4415- AgNPs,  SDT,  CUR,    Examining the Impact of Sonodynamic Therapy With Ultrasound Wave in the Presence of Curcumin-Coated Silver Nanoparticles on the Apoptosis of MCF7 Breast Cancer Cells
- in-vitro, BC, MCF-7
tumCV↓, Curcumin-coated silver nanoparticles (Cur@AgNPs) have shown potential as a sensitizer, demonstrating adverse effects on cancer cell survival.
BAX↑, proapoptotic genes, such as Bax and Caspase-3, increased, while the expression of the antiapoptotic gene Bcl-2 decreased in MCF7 cells treated with the SDT.
Casp3↑,
Bcl-2↓,
eff↑, effect of SDT in the presence of Cur@AgNPs decreases cell viability dependence on US mode
ROS↑, Combined treatment increased the amount of ROS induction
sonoS↑, Higher concentrations of AgNPs (100 μg/ml) acted as acoustic sensitizers and enhanced ROS production
eff↑, Using curcumin as a biological coating reduced the toxicity of AgNPs and improved their significant effects with SDT
MMP↓, reduction in mitochondrial membrane potential (MMP) and the opening of mitochondrial permeability transition pores (mPTPs)
Cyt‑c↑, ultimately facilitating the release of cytochrome c from the mitochondria into the cytosol.

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.

4409- AgNPs,    Plant-based synthesis of gold and silver nanoparticles using Artocarpus heterophyllus aqueous leaf extract and its anticancer activities
- in-vitro, BC, MCF-7
tumCV↓, , AuNPs had no anticancer activity. In contrast, AgNPs showed potent anticancer effects, with inhibitory concentration (IC50) values of 124.626 and 54.981 µg/mL at 48 and 72 hours, respectively.
TumCCA↑, The AgNPs treatment increased the proportion of cells in G2/M phase, indicating the induction of mitotic catastrophe leading to cell death
cycD1/CCND1↓, AgNPs downregulated the expression of several oncogenes associated with cancer cell proliferation and survival (cyclin D1, COX-2, HER-2, and miR622
COX2↓,
HER2/EBBR2↓,

4408- AgNPs,    Chitosan-coated silver nanoparticles synthesized using Moringa oleifera flower extract: A potential therapeutic approach against triple-negative breast cancer
- in-vitro, BC, MDA-MB-231
tumCV↓, The F-Ch-AgNPs had a half-maximal inhibitory concentration (IC50) of 27 ± 0.5 μg/mL

4406- AgNPs,    Silver nanoparticles achieve cytotoxicity against breast cancer by regulating long-chain noncoding RNA XLOC_006390-mediated pathway
- in-vitro, BC, MCF-7 - in-vitro, BC, T47D - in-vitro, BC, MDA-MB-231
TumCD↑, AgNPs showed potent cytotoxicity in breast cancer cells, no matter whether they were tamoxifen sensitive or resistant.
other↓, Next, we found that a long noncoding RNA, XLOC_006390, was decreased in AgNPs-treated breast cancer cells, coupled to inhibited cell proliferation, altered cell cycle and apoptotic phenotype.
P53↑, According to the literature, AgNPs may induce cancer cells apoptosis by activating p53, so as to achieve the antitumor effect
TumCCA↑, We found that AgNPs treatment at 150 μg/ml could induce G0/G1 cell cycle arrest
Apoptosis↑, and promote both early apoptosis and late apoptosis/necrosis rate
ChemoSen↑, AgNPs-based approaches provided a potential way to fight drug resistance and reduce the toxicity related to chemotherapy drugs
tumCV↓, One of the highlights of this study is that AgNPs have strong cytotoxicities on all the breast cancer cell lines and clinically isolated breast cancer cells, with the IC50s at about 150 μg/ml for all
γH2AX↑, early apoptosis markers (γH2AX), was also significantly upregulated by AgNPs treatment
SOX4↓, AgNPs can inhibit the SOX4 expression by regulating XLOC_006390/miR-338-3p axis.

4427- AgNPs,    Silver nanoparticles induce apoptosis and G2/M arrest via PKCζ-dependent signaling in A549 lung cells
- in-vitro, Lung, A549
tumCV↓, Ag NPs reduced cell viability, increased LDH release, and modulated cell cycle distribution through the accumulation of cells at G2/M and sub-G1 phases (cell death)
LDH↑,
TumCCA↑, G2/M and sub-G1 phases (
BAX↑, Ag NP treatment increased Bax and Bid mRNA levels and downregulated Bcl-2 and Bcl-w mRNAs in a dose-dependent manner.
BID↑,
Bcl-2↓,
PKCδ↓, Ag NPs induce strong toxicity and G2/M cell cycle arrest by a mechanism involving PKCζ downregulation in A549 cells.

4428- AgNPs,    p38 MAPK Activation, DNA Damage, Cell Cycle Arrest and Apoptosis As Mechanisms of Toxicity of Silver Nanoparticles in Jurkat T Cells
- in-vitro, AML, Jurkat
toxicity↝, The effect of Ag ions was also investigated and compared with that of AgNPs, as it is anticipated that Ag ions will be released from AgNPs, which may be responsible for their toxicity.
tumCV↓, Cell viability tests indicated high sensitivity of Jurkat T cells when exposed to AgNPs compared to Ag ions
ROS↑, AgNPs and Ag ions induce similar levels of cellular reactive oxygen species during the initial exposure period and; after 24 h, they were increased on exposure to AgNPs compared to Ag ions, which suggest that oxidative stress may be an indirect caus
p38↑, AgNPs exposure activates p38 mitogen-activated protein kinase through nuclear factor-E2-related factor-2 and nuclear factor-kappaB signaling pathways, subsequently inducing DNA damage, cell cycle arrest and apoptosis.
NRF2↓,
NF-kB↝,
DNAdam↑,
Apoptosis↑,

4380- AgNPs,    Silver nanoparticles induce toxicity in A549 cells via ROS-dependent and ROS-independent pathways
- in-vitro, Lung, A549
ROS↑, AgNPs caused ROS formation in the cells
tumCV↓, reduction in their cell viability
MMP↓, and mitochondrial membrane potential (MMP)
TumCCA↑, increase in the proportion of cells in the sub-G1 (apoptosis) population, S phase arrest
PCNA↓, down-regulation of the cell cycle associated proliferating cell nuclear antigen (PCNA) protein
eff↓, Pretreatment of the A549 cells with N-acetyl-cysteine (NAC), an antioxidant, decreased the effects of AgNPs

4370- AgNPs,    Effect of silver nanoparticles in the induction of apoptosis on human hepatocellular carcinoma (HepG2) cell line
- in-vitro, Liver, HepG2
tumCV↓, decreased cell viability in a concentration-dependent manner and the IC50 of 75 μg/mL for Ag NPs
ROS↑, Ag NPs cytotoxicity was associated with induction of ROS and cell apoptosis in HepG2 cell line
Apoptosis↑,

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.

4549- AgNPs,    Silver nanoparticles: Synthesis, medical applications and biosafety
- Review, Var, NA - Review, Diabetic, NA
ROS↑, action mechanisms of AgNPs, which mainly involve the release of silver ions (Ag+), generation of reactive oxygen species (ROS), destruction of membrane structure.
eff↑, briefly introduce a new type of Ag particles smaller than AgNPs, silver Ångstrom (Å, 1 Å = 0.1 nm) particles (AgÅPs), which exhibit better biological activity and lower toxicity compared with AgNPs.
other↝, This method involves reducing silver ions to silver atoms 9, and the process can be divided into two steps, nucleation and growth
DNAdam↑, antimicrobial mechanisms of AgNPs includes destructing bacterial cell walls, producing reactive oxygen species (ROS) and damaging DNA structure
EPR↑, Due to the enhanced permeability and retention (EPR) effect, tumor cells preferentially absorb NPs-sized bodies than normal tissues
eff↑, Large surface area may lead to increased silver ions (Ag+) released from AgNPs, which may enhance the toxicity of nanoparticles.
eff↑, Our team prepared Ångstrom silver particles, capped with fructose as stabilizer, can be stable for a long time
TumMeta↓, AgNPs can induce tumor cell apoptosis through inactivating proteins and regulating signaling pathways, or blocking tumor cell metastasis by inhibiting angiogenesis
angioG↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
*Bacteria↓, Rather than Gram-positive bacteria, AgNPs show a stronger effect on the Gram-negative ones. This may be due to the different thickness of cell wall between two kinds of bacteria
*eff↑, In general, as particle size decreases, the antibacterial effect of AgNPs increases significantly
*AntiViral↑, AgNPs with less than 10 nm size exhibit good antiviral activity 185, 186, which may be due to their large reaction area and strong adhesion to the virus surface.
*AntiFungal↑, Some studies confirm that AgNPs exhibit good antifungal properties against Colletotrichum coccodes, Monilinia sp. 178, Candida spp.
eff↑, The greater cytotoxicity and more ROS production are observed in tumor cells exposed to high positive charged AgNPs
eff↑, Nanoparticles exposed to a protein-containing medium are covered with a layer of mixed protein called protein corona. formation of protein coronas around AgNPs can be a prerequisite for their cytotoxicity
TumCP↓, Numerous experiments in vitro and in vivo have proved that AgNPs can decrease the proliferation and viability of cancer cells.
tumCV↓,
P53↝, gNPs can promote apoptosis by up- or down-regulating expression of key genes, such as p53 242, and regulating essential signaling pathways, such as hypoxia-inducible factor (HIF) pathway
HIF-1↓, Yang et al. found that AgNPs could disrupt the HIF signaling pathway by attenuating HIF-1 protein accumulation and downstream target genes expression
TumCCA↑, Cancer cells treated with AgNPs may also show cell cycle arrest 160, 244
lipid-P↑, Ag+ released by AgNPs induces oxidation of glutathione, and increases lipid peroxidation in cellular membranes, resulting in cytoplasmic constituents leaking from damaged cells
ATP↓, mitochondrial function can be inhibited by AgNPs via disrupting mitochondrial respiratory chain, suppressing ATP production
Cyt‑c↑, and the release of Cyt c, destroy the electron transport chain, and impair mitochondrial function
MMPs↓, AgNPs can also inhibit the progression of tumors by inhibiting MMPs activity.
PI3K↓, Various studies support that AgNPs can deprive cancer cells of both nutrients and oxygen via inhibiting angiogenesis
Akt↓,
*Wound Healing↑, AgNPs exhibit good properties in promoting wound repair and bone healing, as well as inhibition of inflammation.
*Inflam↓,
*Bone Healing↑,
*glucose↓, blood glucose level of diabetic rats decreased when treated with AgNPs for 14 days and 21 days without significant acute toxicity.
*AntiDiabetic↑,
*BBB↑, The small-sized AgNPs are easy to penetrate the body and cross biological barriers like the blood-brain barrier and the blood-testis barrier

346- AgNPs,  RSQ,    Investigating Silver Nanoparticles and Resiquimod as a Local Melanoma Treatment
- in-vivo, Melanoma, SK-MEL-28 - in-vivo, Melanoma, WM35
ROS↑,
Ca+2↝, disrupt mitochondrial homeostasis of Ca2+
Casp3↑, x2-4
Casp8↑, x2-4
Casp9↑, x4-14
CD4+↑,
CD8+↑,
tumCV↓,
eff↓, NAC, an ROS scavenger, could efficiently protect B16.F10 cells from the cytotoxic effects of Ag+ even when exposed to high concentrations of Ag+ (250 μg/ml)
*toxicity↓, non-toxic in mice as evidenced by: 1) no significant change in weights during the study period and 2) no significant increases in the levels of liver enzymes, (ALP), (AST), and ALT

2539- AgNPs,  SDT,    Combined effect of silver nanoparticles and therapeutical ultrasound on ovarian carcinoma cells A2780
- in-vitro, Melanoma, A2780S
tumCV↓, Experimental results indicate a significant decrease of viability of cell, which was affected by the combined action of ultrasound field and silver nanoparticles, compared to the separate exposure of silver nanoparticles or ultrasonic field.
sonoP↑, One of the characteristic effects of sonodynamic therapy is the loosening of cell membranes, thus causing their increased porosity
BioEnh↑,

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

246- AL,    Allicin induces apoptosis of the MGC-803 human gastric carcinoma cell line through the p38 mitogen-activated protein kinase/caspase-3 signaling pathway
- in-vitro, GC, MGC803
Apoptosis↑,
cl‑Casp3↑,
p38↑, In the present study, the protein expression levels of p38 were gradually enhanced in the MGC-803 cells, in response to treatment with 1 μg/ml allicin for 48 h
tumCV↓,
BAX↑, Bax were increased nearly one-fold, whereas the protein expression levels of Bcl-2 level were decreased >35%.
Bcl-2↑,

250- AL,    Allicin Induces p53-Mediated Autophagy in Hep G2 Human Liver Cancer Cells
- in-vitro, Liver, HepG2
P53↓, allicin decreased the level of cytoplasmic p53, the PI3K/mTOR signaling pathway
PI3K↓, decreased the levels of PI3K/mTOR, p-Bcl-2, Bcl-xL, and cytoplasmic p53 in Hep G2 cells.
mTOR↓,
Bcl-2↓,
AMPK↑,
TSC2↑,
Beclin-1↑, llicin increased the levels of Beclin-1, Bad, p-AMPK, TSC2, and Atg7
TumAuto↑, Allicin induced autophagy and increased the formation of autophagosomes and autophagolysosomes in Hep G2 cells.
tumCV↓, Allicin treatment at 35 uM decreased the viability of Hep G2 cells after 12 and 24 h significantly.
ATG7↑,
MMP↓, allicin treatment caused a decrease of MMP of Hep G2 cells and degradation of mitochondria

239- AL,    Allicin induces apoptosis in gastric cancer cells through activation of both extrinsic and intrinsic pathways
- in-vitro, GC, SGC-7901
Apoptosis↑,
Cyt‑c↑, induced cytochrome c release from the mitochondria
Casp3↑,
Casp8↑,
Casp9↑,
BAX↑,
Fas↑,
tumCV↓, 30ug/ml allicin treatment for 48 h reduced tumor cell viability by 70%
DNAdam↑, such as DNA damage, oxidative stress and heat shock proteins
ROS↑,
Telomerase↓, Allicin was shown to induce apoptosis in gastric cancer cells, partly by decreased telomerase activity (21).

5167- AL,    The Effects of Allicin, a Reactive Sulfur Species from Garlic, on a Selection of Mammalian Cell Lines
- in-vitro, Nor, 3T3 - in-vitro, BC, MCF-7 - in-vitro, Lung, A549 - in-vitro, CRC, HT-29
Thiols↓, Garlic produces the thiol-reactive defence substance, allicin, upon wounding.
tumCV↓, Allicin reduced cell viability and cell proliferation in a concentration dependent manner.
TumCP↓, Allicin Inhibits Cell Proliferation
GSH↓, allicin reacts with and depletes the GSH pool.
GSSG↑, Allicin is a thiol-reagent and reacts easily with glutathione, forming S-allylmercaptoglutathione (GSSA) and leading to an increased production of GSSG
ROS↑, Allicin oxidizes thiols and causes oxidative stress in its own right.

3434- ALA,    Alpha lipoic acid modulates metabolic reprogramming in breast cancer stem cells enriched 3D spheroids by targeting phosphoinositide 3-kinase: In silico and in vitro insights
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
tumCV↓, significant dose-dependent reduction in cell viability, with the half-maximal inhibitory concentration (IC50) of LA to be 3.2 mM for MCF-7 cells and 2.9 mM for MDA-MB-231 cells
PI3K↓, LA significantly inhibited PI3K, p-AKT, p-p70S6K and p-mTOR levels
p‑Akt↓,
p‑P70S6K↓,
mTOR↓,
ATP↓, LA markedly reduced both ATP levels and glucose uptake (Fig. 4A and 4B). LA also induced ROS generation in both MCF-7 and MDA-MB231 spheroids
GlucoseCon↓,
ROS↑,
PKM2↓, LA downregulated the expression of PKM2 and LDHA in the spheroids, indicating an inhibition of glycolysis in BCSCs
LDHA↓,
Glycolysis↓,
ChemoSen↑, LA enhances chemosensitivity of spheroids to Dox treatment

3442- ALA,    α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B - in-vitro, Nor, 3T3
tumCV↓, Notably, α‑LA treatment significantly reduced the cell viability, migration, and invasion of PCa cell lines in a dose‑dependent manner.
TumCMig↓,
TumCI↓,
ROS↑, α‑LA supplementation dramatically increased reactive oxygen species (ROS) levels and HIF‑1α expression, which started the downstream molecular cascade and activated JNK/caspase‑3 signaling pathway
Hif1a↑, The expression of HIF-1α significantly increased following α-LA treatment and was comparable with the changes in ROS.
JNK↑,
Casp↑,
TumCCA↑, arrest of the cell cycle in the S‑phase, which has led to apoptosis of PCa cells
Apoptosis↑,
selectivity↑, Also, the treatment of α‑LA improved bone health by reducing PCa‑mediated bone cell modulation.

1007- And,    In vitro and in silico evaluation of Andrographis paniculata ethanolic crude extracts on fatty acid synthase expression on breast cancer cells
- in-vitro, BC, MCF-7 - in-vitro, BC, EMT6
tumCV↓,
i-FASN↓, drastically reduce intracellular FASN protein expression

1536- Api,    Apigenin causes necroptosis by inducing ROS accumulation, mitochondrial dysfunction, and ATP depletion in malignant mesothelioma cells
- in-vitro, MM, MSTO-211H - in-vitro, MM, H2452
tumCV↓,
ROS↑, increase in intracellular reactive oxygen species (ROS)
MMP↓, caused the loss of mitochondrial membrane potential (ΔΨm)
ATP↓, ATP depletion
Apoptosis↑,
Necroptosis↑,
DNAdam↑,
TumCCA↑, delay at the G2/M phase of cell cycle
Casp3↑,
cl‑PARP↑,
MLKL↑,
p‑RIP3↑,
Bax:Bcl2↑,
eff↓, ATP supplementation restored cell viability and levels of DNA damage-, apoptosis- and necroptosis-related proteins that apigenin caused.
eff↓, N-acetylcysteine reduced ROS production and improved ΔΨm loss and cell death that were caused by apigenin.

1563- Api,  MET,    Metformin-induced ROS upregulation as amplified by apigenin causes profound anticancer activity while sparing normal cells
- in-vitro, Nor, HDFa - in-vitro, PC, AsPC-1 - in-vitro, PC, MIA PaCa-2 - in-vitro, Pca, DU145 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
selectivity↑, Metformin increased cellular ROS levels in AsPC-1 pancreatic cancer cells, with minimal effect in HDF, human primary dermal fibroblasts.
selectivity↑, Metformin reduced cellular ATP levels in HDF, but not in AsPC-1 cells
selectivity↓, Metformin increased AMPK, p-AMPK (Thr172), FOXO3a, p-FOXO3a (Ser413), and MnSOD levels in HDF, but not in AsPC-1 cells
ROS↑,
eff↑, Metformin combined with apigenin increased ROS levels dramatically and decreased cell viability in various cancer cells including AsPC-1 cells, with each drug used singly having a minimal effect.
tumCV↓,
MMP↓, Metformin/apigenin combination synergistically decreased mitochondrial membrane potential in AsPC-1 cells but to a lesser extent in HDF cells
Dose∅, co-treatment with metformin (0.05, 0.5 or 5 mM) and apigenin (20 µM) dramatically increased cellular ROS levels in AsPC-1 cells
eff↓, NAC blocked the metformin/apigenin co-treatment-induced cell death in AsPC-1 cells
DNAdam↑, Combination of metformin and apigenin leads to DNA damage-induced apoptosis, autophagy and necroptosis in AsPC-1 cells but not in HDF cells
Apoptosis↑,
TumAuto↑,
Necroptosis↑,
p‑P53↑, p-p53, Bim, Bid, Bax, cleaved PARP, caspase 3, caspase 8, and caspase 9 were also significantly increased by combination of metformin and apigenin in AsPC-1
BIM↑,
BAX↑,
p‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
Cyt‑c↑, Cytochrome C was also released from mitochondria in AsPC-1 cell
Bcl-2↓,
AIF↑, Interestingly, autophagy-related proteins (AIF, P62 and LC3B) and necroptosis-related proteins (MLKL, p-MLKL, RIP3 and p-RIP3) were also increased by combination of metformin and apigenin
p62↑,
LC3B↑,
MLKL↑,
p‑MLKL↓,
RIP3↑,
p‑RIP3↑,
TumCG↑, in vivo
TumW↓, metformin (125 mg/kg) or apigenin (40 mg/kg) caused a reduction of tumor size compared to the control group (Fig. 7D). However, oral administration of combination of metformin and apigenin decreased tumor weight profoundly

1008- Api,    Apigenin-induced lysosomal degradation of β-catenin in Wnt/β-catenin signaling
- in-vitro, CRC, HCT116 - in-vitro, CRC, SW480
Wnt/(β-catenin)↓,
β-catenin/ZEB1↓,
TumAuto↑,
Akt↓,
mTOR↓,
tumCV↓,
TumCCA↑, cell cycle arrest at G2/M phase
TumAuto↑, data suggested the involvement of autophagy in apigenin-induced β-catenin down-regulation during Wnt signaling
p‑Akt↓,
p‑p70S6↓,
p‑4E-BP1↓,

1024- Api,  CUR,    Apigenin suppresses PD-L1 expression in melanoma and host dendritic cells to elicit synergistic therapeutic effects
- vitro+vivo, Melanoma, A375 - in-vitro, Melanoma, A2058 - in-vitro, Melanoma, RPMI-7951
TumCG↓,
Apoptosis↑,
PD-L1↓, IFN-γ-induced PD-L1 upregulation was significantly inhibited by flavonoids, especially apigenin
STAT1↓,
tumCV↓,
T-Cell↑, Curcumin and apigenin enhance T cell-mediated melanoma cell killing

5137- ART/DHA,    Autophagy-dependent cell cycle arrest in esophageal cancer cells exposed to dihydroartemisinin
- vitro+vivo, ESCC, Eca109
tumCV↓, Our results proved that DHA significantly reduced the viability of Eca109 cells in a dose- and time-dependent manner.
TumCCA↑, DHA evidently induced cell cycle arrest at the G2/M phase in Eca109 cells
ROS↑, Mechanistically, DHA induced intracellular ROS generation and autophagy in Eca109 cells
TumAuto↑,
eff↓, blocking ROS by an antioxidant NAC obviously inhibited autophagy
TRF2↓, we found that telomere shelterin component TRF2 was down-regulated in Eca109 cells exposed to DHA through autophagy-dependent degradation
TumCP↓, DHA inhibits the proliferation ability of Eca109 cells in vitro and in vivo

5133- ART/DHA,    Dihydroartemisinin Exerts Anti-Tumor Activity by Inducing Mitochondrion and Endoplasmic Reticulum Apoptosis and Autophagic Cell Death in Human Glioblastoma Cells
- in-vitro, GBM, U87MG - in-vitro, GBM, U251
AntiTum↑, (DHA) has been shown to exhibit anti-tumor activity in various cancer cells.
tumCV↓, Our results proved that DHA treatment significantly reduced cell viability in a dose- and time-dependent manner by CCK-8 assay.
Apoptosis↓, DHA induced apoptosis of GBM cells through mitochondrial membrane depolarization, release of cytochrome c and activation of caspases-9.
MMP↓,
Cyt‑c↑,
Casp9↑,
CHOP↑, Enhanced expression of GRP78, CHOP and eIF2α and activation of caspase 12 were additionally confirmed that endoplasmic reticulum (ER) stress pathway of apoptosis
GRP78/BiP↑,
eIF2α↑,
Casp12↑,
ER Stress↑, DHA Induced Apoptosis through Mitochondria and Endoplasmic Reticulum (ER) Stress Pathways of Apoptosis in Human GBM Cells
TumAuto↑, ER stress and mitochondrial dysfunction were involved in the DHA-induced autophagy.
ROS↑, Further study revealed that accumulation of reactive oxygen species (ROS) was attributed to the DHA induction of apoptosis and autophagy.

5130- ART/DHA,    Dihydroartemisinin Induces Apoptosis in Human Bladder Cancer Cell Lines Through Reactive Oxygen Species, Mitochondrial Membrane Potential, and Cytochrome C Pathway
- in-vitro, Bladder, T24/HTB-9
tumCV↓, DHA significantly reduced cell viability in a dose-dependent manner.
eff↓, Cytotoxicity of DHA was suppressed by N-acetylcysteine (NAC)
Apoptosis↑, induction of cell apoptosis, which were manifested by annexin V-FITC staining, activation of caspase-3
Casp3↑,
ROS↑, DHA also increased ROS generation, cytochrome c release, and loss of mitochondrial transmembrane potential (ΔΨm) in cells.
Cyt‑c↑,
MMP↓,
Bcl-2↓, downregulation of regulatory protein Bcl-2 and upregulation of Bax protein by DHA were also observed
BAX↑,
MOMP↑, Dihydroartemisinin increases mitochondrial permeability of EJ-138 and HTB-9 cells by Collapse of ΔΨm
TumCG↓, It has shown that DHA selectively inhibits the growth of many cancer cells types, such as leukemia,[29] pancreas,[30] breast[31] and prostate[32] cancers

2576- ART/DHA,  AL,    The Synergistic Anticancer Effect of Artesunate Combined with Allicin in Osteosarcoma Cell Line in Vitro and in Vivo
- in-vitro, OS, MG63 - in-vivo, NA, NA
eff↑, Our results indicated that artesunate and allicin in combination exert synergistic effects on osteosarcoma cell proliferation and apoptosis.
tumCV↓,
Casp3↑, apoptotic rate was significantly increased through caspase-3/9 expression and activity enhancement
Casp9↑,
Apoptosis↑,
TumCG↓, Combination suppresses in vivo tumor growth

1369- Ash,    Withaferin A inhibits cell proliferation of U266B1 and IM-9 human myeloma cells by inducing intrinsic apoptosis
- in-vitro, Melanoma, U266
tumCV↓,
Apoptosis↑,
BAX↑,
Cyt‑c↑,
Bcl-2↓,
cl‑PARP↑,
cl‑Casp3↑,
cl‑Casp9↑,
ROS↑,
eff↓, treatment of the U266B1 and IM-9 with ascorbic acid (antioxidant) could prevent the withaferin A mediated ROS production and the withaferin A induced antiproliferative effects.

1368- Ash,  Cisplatin,    Withania somnifera Root Extract Enhances Chemotherapy through ‘Priming’
- in-vitro, Colon, HT-29 - in-vitro, BC, MDA-MB-231
tumCV↓,
*toxicity↓, However, in non-cancer cells (MCF10A) there was no reduction in cell viability compared to non-treatment
ROS↑, only in cancer cells ****
mitResp↓,
ChemoSen↑, ‘Priming’ with W. somnifera (treatment: 48 h prior to 100 μM cisplatin)

1433- Ash,  SFN,    A Novel Combination of Withaferin A and Sulforaphane Inhibits Epigenetic Machinery, Cellular Viability and Induces Apoptosis of Breast Cancer Cells
- in-vitro, BC, MCF-7 - in-vitro, BC, MDA-MB-231
eff↑, synergistic inhibition of cellular viability in MCF-7
Bcl-2↓,
BAX↑,
tumCV↓,
DNMT1↓,
DNMT3A↓, DNMT3A and DNMT3B mRNA expression is down-regulated
HDAC↓, significant decreases in HDAC activity

5389- AsP,  Tras,    ASCORBYL PALMITATE ENHANCES ANTI-PROLIFERATIVE EFFECT OF TRASTUZUMAB IN HER2-POSITIVE BREAST CANCER CELLS
tumCV↓, AP reduced cell viability in a time- and dose-dependent manner, and its combination with trastuzumab further decreased cell viability.
eff↑, A cytometric analysis showed enhanced apoptosis after combination treatment
P53↑, mRNA analysis revealed upregulated TP53 mRNA expression, along with upregulation of BAX, CYCS, CASP3, and CASP8 gene expression, while the BCL-2 and BCL2L1 genes were downregulated, further supporting the induction of apoptosis.
BAX↑,
Casp3↑,
Casp8↑,
Bcl-2↓,
Apoptosis↑,
p‑p38↓, Western blot assay, which showed suppression of phospho-P38, ERK1/2, and PI3K protein synthesis.
ERK↓,
PI3K↓,

4822- ASTX,  Rad,    Astaxanthin Synergizes with Ionizing Radiation (IR) in Oral Squamous Cell Carcinoma (OSCC)
tumCV↓, ATX inhibited viability of OSCC cells but not NHOK.
selectivity↑,
RadioS↑, In OSCC cells, ATX further enhanced the cell death induced by IR.
GPx4↓, ATX could synergize with IR, further inhibiting GPX4, SLC7A11 and promoting ACSL4 in OSCC cells.
Ferroptosis↑, ATX might synergize with IR treatment in OSCC partly via ferroptosis.

4818- ASTX,  MEL,    Effect of astaxanthin and melatonin on cell viability and DNA damage in human breast cancer cell lines
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, T47D - in-vitro, Nor, MCF10
TumCD↑, Astaxanthin increases the melatonin-induced cell death in breast cancer cells
DNAdam↑, Astaxanthin-melatonin combination and DNA damages in breast cancer cells
*antiOx↑, strong anti-oxidative, anti-tumoral, and anti-inflammatory effects.
*AntiTum↑,
Inflam↓,
tumCV↓, Astaxanthin at lower doses than melatonin reduced cell viability and Bcl2 expression, induced apoptosis and DNA damage in MDA-MB-231 and T47D.
Bcl-2↓,
Apoptosis↓,
selectivity↑, Meanwhile, the effects of astaxanthin on cell cytotoxicity, apoptosis, and DNA damage in MCF10A cells are insignificant compared to MDA-MB-231 and T47D.
eff↑, Furthermore, the presence of astaxanthin increased the function of melatonin-induced cell death in breast cancer cells.
Dose↓, The results showed that very low doses of astaxanthin reduced survival rate, induced apoptosis, reduced the expression of Bcl2 proteins, and destroyed the DNA in cancerous cells

4809- ASTX,    Astaxanthin Inhibits Proliferation of Human Gastric Cancer Cell Lines by Interrupting Cell Cycle Progression
- in-vitro, GC, AGS - in-vitro, GC, MKN45
tumCV↓, The viability of each cancer cell line was suppressed by astaxanthin in a dose-dependent manner with significantly decreased proliferation in KATO-III and SNU-1 cells.
TumCP↓,
TumCCA↑, Astaxanthin inhibits proliferation by interrupting cell cycle progression in KATO-III and SNU-1 gastric cancer cells.
p‑ERK↓, This may be caused by the inhibition of the phosphorylation of ERK and the enhanced expression of p27kip-1.
p27↑,
cycD1/CCND1↓, Astaxanthin downregulates p-ERK level in tumor cells, inhibiting the cyclin D1/CDK4 complex
CDK4↓,

5451- ATV,    In vitro and in vivo anticancer effects of mevalonate pathway modulation on human cancer cells
- in-vitro, BC, MDA-MB-231 - in-vitro, GBM, U87MG - in-vitro, GBM, A172
TumAuto↑, cerivastatin, pitavastatin, and fluvastatin were the most potent anti-proliferative, autophagy inducing agents in human cancer cells including stem cell-like primary glioblastoma cell lines.
CSCs↓,
HMG-CoA↓, These data demonstrate that statins main effect is via targeting the mevalonate synthesis pathway in tumour cells.
TumCP↓, Statins inhibit proliferation/viability of human tumour cell lines
tumCV↓,
TumCCA↑, Statins induce cell cycle arrest in tumour cells
TumCG↓, Statins inhibit tumour growth in animal models
HMGCR↓, Statins are competitive inhibitors of HMGCR, which converts HMG-CoA to mevalonate.

5366- AV,    Aloe vera: A review of toxicity and adverse clinical effects
- Review, Var, NA
*Dose↝, Chemical analysis reveals that the Aloe plant contains various polysaccharides and phenolic chemicals, notably anthraquinones.
*toxicity↝, lethal dose (LD50) in Swiss albino mice was 120.65 mg/kg.
tumCV↓, Aloe vera whole-leaf material caused a dose-dependent decrease in the viability in HeLa and HepG2 cells
*AntiAg↑, Aloe vera have antiplatelet effects,

5369- AV,    Assessment of Anticancer Effects of Aloe vera on 3D Liver Tumor Spheroids in a Microfluidic Platform
- in-vitro, Liver, HepG2
tumCV↓, The results indicated that Aloe vera markedly diminished cell viability by triggering apoptosis at concentrations over 12.5 mg/mL.
AntiCan↑, This study underscores the promise of Aloe vera as a natural anticancer agent and illustrates the efficacy of microfluidic platforms for enhanced drug screening and customized medicine applications.
P53↑, This extract upregulated the P53 tumor suppressor gene and downregulated the Bcl‐2 antiapoptotic gene, indicating its potential to induce cancer cell death in both HepG2 and MCF7 cells
Bcl-2↓,

5250- Ba,    Exploring baicalein: A natural flavonoid for enhancing cancer prevention and treatment
- Review, Var, NA
Apoptosis↑, Baicalein is thought to prevent cancer progression by inducing apoptosis, autophagy, and genome instability, and its ability to promote chemo-potentiation, anti-metastatic effects, and regulate specific signalling molecules and transcription factors.
TumAuto↑,
DNAdam↑,
*antiOx↑, Baicalein has already been proven to be a radical scavenger that acts as an antioxidant [14,15
Inflam↓, it can also reduce inflammation [16] and act as an E2 prostaglandin inhibitor [17].
PGE2↓,
TumCCA↑, Baicalein properties prevent cell proliferation, induce apoptosis, autophagy, cell cycle arrest, cancer cell migration and invasion, and decrease angiogenesis [18,19].
TumCMig↓,
TumCI↓,
angioG↓,
selectivity↑, Furthermore, some studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells.
ChemoSen↑, the current review emphasises baicaleins' synergistic potential with other chemotherapeutic agents
HIF-1↓, baicalein against ovarian cancer by demonstrating that it can limit tumour cell viability by downregulating the expression of cancer-promoting genes such as HIF-1, cMyc, NFkB, and VEGF
cMyc↓,
NF-kB↓,
VEGF↓,
P53↑, Baicalein has been shown to activate p53, a tumour suppressor protein that regulates cell growth and division [26].
MMP2↓, anticancer properties of baicalein are mediated through various molecular mechanisms, including inhibition of MMP-2;
CSCs↓, inhibition of cancer stem cells
Bcl-xL↓, after bladder cancer cells were treated with baicalein, the expression of antiapoptotic genes (Bcl2, Bcl-xL, XIAP, and survivin) was reduced, and cell viability was decreased [38].
XIAP↓,
survivin↓,
tumCV↓,
Casp3↑, upregulating the expression of caspase-3 and caspase-8 and decreased the BCL-2/BAX ratio [16]
Casp8↑,
Bax:Bcl2↑,
Akt↓, in lung cancer cells, apoptosis was induced through the downregulation of the Akt/mTOR signalling pathway [25].
mTOR↓,
PCNA↓, baicalein treatment promoted apoptosis in mice with U87 gliomas by downregulating PCNA expression, enhancing the expression of caspase-3 and caspase-9 and improving the Bax/Bcl-2 ratio
MMP↓, baicalein treatment of lung cancer cells caused a collapse of the mitochondrial membrane potential (MMP), an increase in ROS generation, and enhanced PARP, caspase 3, and caspase 9 cleavage,
ROS↑,
PARP↑,
Casp9↑,
BioAv↑, Baicalein has been found to enhance the cytotoxicity and bioavailability of certain cancer therapy drugs when combined [85]
eff↑, combination of baicalein with silymarin differentially decreased the viability of HepG2 cells, enhanced the proportion of cells in the G0/G1 phase, upregulated tumour suppressors such as Rb and p53 and CDK inhibitors, and downregulated cyclin D1, cyc
P-gp↓, By inhibiting P-glycoprotein (P-gp), baicalein can increase the accumulation of chemotherapeutic drugs within cancer cells [21]
BioAv↑, selenium–baicalein nanoparticles as a targeted therapeutic strategy for NSCLC. This strategy significantly improves the bioavailability of baicalein through several mechanisms.
selectivity↑, ome studies have suggested that baicalein has a lower toxicity on normal cells than cancer cells, indicating some selectivity for cancer cells

1529- Ba,    Studies on the Inhibitory Mechanisms of Baicalein in B16F10 Melanoma Cell Proliferation
- in-vitro, Melanoma, B16-F10
ROS↑,
eff↓, ROS scavengers effectively reversed cell viability reduction induced by baicalein
tumCV↓,
Casp3↑,
necrosis↑,

1533- Ba,    Baicalein, as a Prooxidant, Triggers Mitochondrial Apoptosis in MCF-7 Human Breast Cancer Cells Through Mobilization of Intracellular Copper and Reactive Oxygen Species Generation
- in-vitro, BrCC, MCF-7 - in-vitro, Nor, MCF10
tumCV↓,
i-ROS↑, enhancement the level of intracellular ROS exhibit pro-oxidant activity in the presence of copper ions
MMP↓,
Bcl-2↓,
BAX↑,
Cyt‑c↑, release of cytochrome C
Casp9↑,
Casp3↑,
eff↓, The pretreatment with NeoCu (I)-specific chelator) remarkably weakened these effects of baicalein exhibit pro-oxidant activity in the presence of copper ions
selectivity↑, baicalein presented little cytotoxicity to normal breast epithelial cells
*toxicity∅, baicalein presented little cytotoxicity to normal breast epithelial cells. explained by the undetectable levels of copper present in MCF-10A cells.
Apoptosis↑,
Fenton↑, results are in further support that the prooxidant action of baicalein involves the reduction of Cu (II) to Cu (I), and the consequent generation of hydroxyl radicals.


Showing Research Papers: 1 to 50 of 315
Page 1 of 7 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 315

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Fenton↑, 1,   Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   GSH∅, 1,   GSSG↑, 1,   HO-2↑, 1,   lipid-P↑, 1,   NRF2↓, 1,   ROS↑, 26,   i-ROS↑, 1,   Thiols↓, 1,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   ATP↓, 4,   mitResp↓, 1,   MMP↓, 10,   MMP↑, 1,   mtDam↑, 1,   XIAP↓, 1,  

Core Metabolism/Glycolysis ⓘ

AMPK↑, 1,   ATG7↑, 1,   cMyc↓, 1,   cMyc↑, 1,   i-FASN↓, 1,   GlucoseCon↓, 1,   GlucoseCon∅, 1,   Glycolysis↓, 1,   HMG-CoA↓, 1,   lactateProd∅, 1,   LDH↓, 2,   LDH↑, 1,   LDHA↓, 1,   PKM2↓, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 3,   p‑Akt↓, 2,   Apoptosis↓, 2,   Apoptosis↑, 20,   Bak↑, 1,   BAX↑, 11,   Bax:Bcl2↑, 2,   Bcl-2↓, 11,   Bcl-2↑, 1,   Bcl-xL↓, 1,   BID↑, 1,   BIM↑, 1,   Casp↑, 2,   Casp12↑, 1,   Casp3↑, 12,   cl‑Casp3↑, 2,   Casp8↑, 5,   Casp9↑, 7,   cl‑Casp9↑, 1,   Cyt‑c↑, 8,   Fas↑, 1,   Ferroptosis↑, 1,   JNK↑, 1,   MLKL↑, 2,   p‑MLKL↓, 1,   MOMP↑, 1,   Necroptosis↑, 2,   necrosis↑, 1,   p27↑, 1,   p38↑, 2,   p‑p38↓, 1,   survivin↓, 1,   Telomerase↓, 1,   TumCD↑, 3,  

Kinase & Signal Transduction ⓘ

HER2/EBBR2↓, 1,   p‑p70S6↓, 1,   TSC2↑, 1,  

Transcription & Epigenetics ⓘ

other↓, 1,   other↝, 1,   sonoS↑, 1,   tumCV↓, 50,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   eIF2α↑, 1,   ER Stress↑, 2,   GRP78/BiP↑, 1,   HSP70/HSPA5↓, 1,   UPR↑, 1,  

Autophagy & Lysosomes ⓘ

Beclin-1↑, 1,   LC3B↑, 1,   p62↑, 1,   TumAuto↑, 8,  

DNA Damage & Repair ⓘ

DNAdam↑, 10,   DNMT1↓, 1,   DNMT3A↓, 1,   P53↓, 1,   P53↑, 4,   P53↝, 1,   p‑P53↑, 1,   PARP↑, 1,   p‑PARP↑, 1,   cl‑PARP↑, 2,   PCNA↓, 2,   γH2AX↑, 1,  

Cell Cycle & Senescence ⓘ

CDK4↓, 1,   cycD1/CCND1↓, 2,   TumCCA↑, 14,  

Proliferation, Differentiation & Cell State ⓘ

p‑4E-BP1↓, 1,   CSCs↓, 4,   ERK↓, 1,   p‑ERK↓, 1,   HDAC↓, 1,   HMGCR↓, 1,   mTOR↓, 4,   p‑P70S6K↓, 1,   PI3K↓, 4,   STAT1↓, 1,   TRF2↓, 1,   TumCG↓, 4,   TumCG↑, 1,   Wnt/(β-catenin)↓, 1,  

Migration ⓘ

Ca+2↝, 1,   MMP2↓, 1,   MMPs↓, 1,   PKCδ↓, 1,   RIP3↑, 1,   p‑RIP3↑, 2,   SOX4↓, 1,   TumCI↓, 2,   TumCMig↓, 3,   TumCP↓, 5,   TumMeta↓, 1,   β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 2,   EPR↑, 2,   HIF-1↓, 2,   Hif1a↑, 1,   VEGF↓, 1,  

Barriers & Transport ⓘ

P-gp↓, 1,   sonoP↑, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↑, 1,   COX2↓, 1,   Inflam↓, 3,   NF-kB↓, 1,   NF-kB↝, 1,   PD-L1↓, 1,   PGE2↓, 1,   T-Cell↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 2,   BioEnh↑, 1,   ChemoSen↑, 5,   Dose↓, 1,   Dose↝, 1,   Dose∅, 1,   eff↓, 12,   eff↑, 16,   RadioS↑, 1,   selectivity↓, 1,   selectivity↑, 16,  

Clinical Biomarkers ⓘ

HER2/EBBR2↓, 1,   LDH↓, 2,   LDH↑, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

AntiCan↑, 8,   AntiTum↑, 1,   chemoP↑, 1,   toxicity↓, 1,   toxicity↝, 1,   TumW↓, 1,  

Infection & Microbiome ⓘ

Bacteria↓, 1,   CD8+↑, 1,  
Total Targets: 165

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 2,   ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

glucose↓, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,  

Migration ⓘ

AntiAg↑, 1,  

Barriers & Transport ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   eff↑, 1,  

Functional Outcomes ⓘ

AntiDiabetic↑, 1,   AntiTum↑, 1,   Bone Healing↑, 1,   toxicity↓, 2,   toxicity↝, 1,   toxicity∅, 1,   Wound Healing↑, 1,  

Infection & Microbiome ⓘ

AntiFungal↑, 1,   AntiViral↑, 1,   Bacteria↓, 2,  
Total Targets: 19

Scientific Paper Hit Count for: tumCV, Cell Viability
20 Silver-NanoParticles
15 Quercetin
12 Curcumin
12 Sulforaphane (mainly Broccoli)
12 Thymoquinone
10 Cisplatin
9 Honokiol
9 Phenethyl isothiocyanate
8 Betulinic acid
7 SonoDynamic Therapy UltraSound
7 Berberine
7 Capsaicin
7 Shikonin
6 Allicin (mainly Garlic)
6 Carvacrol
6 Resveratrol
6 Fisetin
6 Magnetic Fields
5 Radiotherapy/Radiation
4 Apigenin (mainly Parsley)
4 Metformin
4 Artemisinin
4 Baicalein
4 Berbamine
4 Biochanin A
4 Gemcitabine (Gemzar)
4 Caffeic Acid Phenethyl Ester (CAPE)
4 Emodin
4 Shilajit/Fulvic Acid
4 Graviola
4 Propolis -bee glue
4 Rosmarinic acid
4 Silymarin (Milk Thistle) silibinin
4 Vitamin C (Ascorbic Acid)
3 Ashwagandha(Withaferin A)
3 Astaxanthin
3 Carnosic acid
3 5-fluorouracil
3 chitosan
3 Selenium
3 Chrysin
3 Citric Acid
3 Gallic acid
3 Magnolol
3 Hyperthermia
3 doxorubicin
3 Juglone
3 Lycopene
3 Methylene blue
3 Magnetic Field Rotating
3 Piperlongumine
3 Parthenolide
3 Selenite (Sodium)
3 Urolithin
2 Alpha-Lipoic-Acid
2 Aloe anthraquinones
2 Bacopa monnieri
2 Boswellia (frankincense)
2 brusatol
2 Caffeic acid
2 Chlorogenic acid
2 Coenzyme Q10
2 Copper and Cu NanoParticles
2 Hydroxycinnamic-acid
2 Dichloroacetate
2 EGCG (Epigallocatechin Gallate)
2 Gambogic Acid
2 Garcinol
2 Luteolin
2 Iron
2 Gold NanoParticles
2 Methylsulfonylmethane
2 Naringin
2 Nimbolide
2 Piperine
2 Plumbagin
2 salinomycin
2 polyethylene glycol
2 Selenium NanoParticles
2 Chemotherapy
2 Photodynamic Therapy
2 Aflavin-3,3′-digallate
2 Ursolic acid
2 VitK3,menadione
2 Zerumbone
1 3-bromopyruvate
1 Resiquimod
1 Andrographis
1 Ascorbyl Palmitate
1 Trastuzumab
1 Melatonin
1 Atorvastatin
1 Bevacizumab (brand Avastin)
1 borneol
1 Boron
1 Catechins
1 Cannabidiol
1 Selenate
1 Vitamin E
1 Ellagic acid
1 Electrical Pulses
1 Fucoidan
1 Ferulic acid
1 Ginkgo biloba
1 HydroxyCitric Acid
1 tamoxifen
1 HydroxyTyrosol
1 itraconazole
1 Folic Acid, Vit B9
1 immunotherapy
1 Mushroom Chaga
1 Bicarbonate(Sodium)
1 Niclosamide (Niclocide)
1 Oleuropein
1 Propyl gallate
1 Pterostilbene
1 Hyperoside
1 Scoulerine
1 acetazolamide
1 Vitamin D3
1 Vitamin K2
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#:897  State#:%  Dir#:1
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