TumCCA Cancer Research Results

TumCCA, Tumor cell cycle arrest: Click to Expand ⟱

Source:

Type:

Tumor cell cycle arrest refers to the process by which cancer cells stop progressing through the cell cycle, which is the series of phases that a cell goes through to divide and replicate. This arrest can occur at various checkpoints in the cell cycle, including the G1, S, G2, and M phases. S, G1, G2, and M are the four phases of mitosis.

Scientific Papers found: Click to Expand⟱

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,

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.

1000-

AG,

5-FU,

Characterization and anti-tumor bioactivity of astragalus polysaccharides by immunomodulation

vitro+vivo,

BC,

4T1

TumCG↓,
TumCCA↑, cell cycle arrest (G2 phase)
Apoptosis↑,
*IL2↑, in peripheral blood
*TNF-α↑, in peripheral blood
*IFN-γ↑, in peripheral blood

5431-

AG,

Advances in research on the anti-tumor mechanism of Astragalus polysaccharides

Review,

Var,

AntiTum↑, APS has been increasingly used in cancer therapy owing to its anti-tumor ability as it prevents the progression of prostate, liver, cervical, ovarian, and non-small-cell lung cancer by suppressing tumor cell growth and invasion and enhancing apoptosi
TumCG↓,
TumCI↓,
Apoptosis↑, after APS treatment, the apoptosis of HepG2 cells is accelerated (57).
Imm↑, APS enhances the sensitivity of tumors to antineoplastic agents and improves the body’s immunity
Bcl-2↓, Huang et al. proposed that APS induces H22 (a hepatocellular cancer [HCC] cell line) apoptosis by downregulating Bcl-2 and upregulating Bax expression (56).
BAX↑,
Wnt↓, downregulating the Wnt/β-catenin signaling pathway.
β-catenin/ZEB1↓,
TumCG↓, APS effectively inhibited the growth of MDA-MB-231 (a human breast cancer [BC] cell line) graft tumor (58)
miR-133a-3p↑, apoptosis rate of human osteosarcoma MG63 cells increased owing to the upregulation of miR-133a and inactivation of the JNK signaling pathways (71).
JNK↓,
Fas↑, Li and Shen found that APS can induce apoptosis by activating the Fas death receptor pathway.
P53↑, Zhang et al. showed that APS could activate p53 and p21 and inhibit the expression of Notch1 and Notch3 in vitro, ultimately inhibiting cell proliferation and promoting their apoptosis
P21↑,
NOTCH1↓,
NOTCH3↓,
TumCP↓,
TumCCA↑, Liu et al. found that APS induced the cell cycle of bladder cancer UM-UC-3 to stop in the G0/G1 phase, thus inhibiting its proliferation
GPx4↓, APS was found to reduce GPX4 expression, inhibit the activity of the light chain subunit SLC7A11 (xCT), and promote the formation of BECN1-xCT complex by activating AMPK/BECN1 signaling.
xCT↓,
AMPK↑,
Beclin-1↑,
NF-kB↓, APS could control the proliferation of lung cancer cells (A549 and NCI-H358 cells) by inhibiting the NF-κB signaling pathway (97)
EMT↓, APS treatment led to reduced EMT markers (vimentin, AXL) and MIF levels in cells.
Vim↓,
TumMeta↓, APS inhibits Lewis lung cancer growth and metastasis in mice by significantly reducing VEGF and EGFR expression in cancerous tissues
VEGF↓,
EGFR↓,
eff↑, Nano-drug delivery systems can increase efficiency and reduce toxicity
eff↑, Jiao et al. developed selenium nanoparticles modified with macromolecular weight APS and observed positive results in hepatoma treatment
MMP↓, Subsequent investigations revealed that APS can decrease the ΔΨm values and Bcl-2, p-PI3K, P-gp, and p-AKT levels while elevating Bax expression.
P-gp↓,
MMP9↓, downregulation of MMP-9 expression,
ChemoSen↑, Li et al. observed that APS could enhance the sensitivity of SKOV3 ovarian cancer cells to CDDP treatment by activating the mitochondrial apoptosis pathway and JNK1/2 signaling pathway
SIRT1↓, APS significantly suppressed SIRT1 and SREBP1 expression, decreased cholesterol and triglyceride levels in PC3 and DU145, and attenuated cell proliferation.
SREBP1↓,
TumAuto↑, APS can induce autophagy in colorectal cancer cells by inhibiting the PI3K/AKT/mTOR axis and the development of cancer cells.
PI3K↓,
mTOR↓,
Casp3↑, Shen found that APS elevated caspase-9, caspase-3, and Bax protein levels, decreased Bcl-2 protein expression, and inhibited CD133 and CD44 co-positive colon cancer stem cell proliferation time
Casp9↑,
CD133↓,
CD44↓,
CSCs↓,
QoL↑, QOL was significantly improved as indicated by the reduction in pain and improvement in appetite

5434-

AG,

Recent Advances in the Mechanisms and Applications of Astragalus Polysaccharides in Liver Cancer Treatment: An Overview

Review,

Liver,

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

4414-

AgNPs,

Silver nanoparticles: Forging a new frontline in lung cancer therapy

Review,

Lung,

tumCV↑, AgNPs exhibit significant cytotoxic and apoptotic effects in lung cancer cell lines through mechanisms involving gene regulation, reactive oxygen species (ROS) production, and mitochondrial depolarization.
ROS↑,
MMP↓,
TumCCA↑, dose-dependent reductions in cell viability, cell cycle arrest, and apoptosis induction.
Apoptosis↑,
angioG↓, inhibit angiogenesis

4417-

AgNPs,

Caffeine-boosted silver nanoparticles target breast cancer cells by triggering oxidative stress, inflammation, and apoptotic pathways

in-vitro,

BC,

MDA-MB-231

ROS↑, Caf-AgNPs significantly increased ROS, malondialdehyde, COX-2, IL-1β, and TNF-α level in BC cells, which was accompanied by a decrease in glutathione levels.
MDA↑,
COX2↑,
IL1β↑,
TNF-α↑,
GSH↓,
Cyt‑c↑, increased levels of cytosolic cytochrome c, caspase-3, and Bax proteins, as well as a significant decrease in Bcl-2 expression and Bcl-2/Bax ratio
Casp3↑,
BAX↑,
Bcl-2↓,
LDH↓, Cancer cells subjected to Caf-AgNPs demonstrated elevated lactate dehydrogenase (LDH) membrane leakage
cycD1/CCND1↓, notable downregulation of cyclin D1 and cyclin-dependent kinase 2 (CDK2) mRNA expression
CDK2↓,
TumCCA↑, several mechanisms for cellular destruction, including cell cycle arrest, oxidative stress induction, modulation of the inflammatory response, and mitochondrial apoptosis
mt-Apoptosis↑,

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.

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

12.75 nm

54.981 µg/mL

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↓,

4406-

AgNPs,

Silver nanoparticles achieve cytotoxicity against breast cancer by regulating long-chain noncoding RNA XLOC_006390-mediated pathway

in-vitro,

BC,

MCF-7

63.1 ± 8.3 nm

tissues from 64 patients

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.

4435-

AgNPs,

Gluc,

Glucose-Functionalized Silver Nanoparticles as a Potential New Therapy Agent Targeting Hormone-Resistant Prostate Cancer cells

in-vitro,

Pca,

PC3

average size of 61nm

911ug/mL

in-vitro,

Pca,

LNCaP

in-vitro,

Pca,

DU145

1579ug/mL

selectivity↑, Both AgNPs and G-AgNPs were cytotoxic only to CRPC cells and not to hormone-sensitive ones and their effect was higher after functionalization showing the potential of glucose to favor AgNPs’ uptake by cancer cells.
ROS↑, NPs increased the ROS, inducing mitochondrial damage, and arresting cell cycle in S Phase, therefore blocking proliferation, and inducing apoptosis.
mtDam↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
MMP↓, AgNPs were able to depolarize the cells’ mitochondria to 32.74% and 10.36%, respectively

4436-

AgNPs,

Silver Nanoparticles (AgNPs) as Enhancers of Everolimus and Radiotherapy Sensitivity on Clear Cell Renal Cell Carcinoma

in-vitro,

Kidney,

786-O

61 ± 10 nm

AgNP doses ranging from 500 to 3000 µg/mL for 24 h

ROS↑, AgNPs are cytotoxic to 786-O cells, a ccRCC cell line, entering through endocytosis, increasing ROS, depolarizing mitochondrial membrane, and blocking the cell cycle, leading to a reduction of proliferation capacity and apoptosis.
MMP↑,
TumCCA↑,
TumCP↓,
Apoptosis↑,
RadioS↑, 786-O is intrinsically resistant to radiation, but after AgNPs’ administration, radiation induces cytotoxicity through mitochondrial membrane depolarization and S phase blockage.

4438-

AgNPs,

ART/DHA,

Biogenic synthesis of AgNPs using Artemisia oliveriana extract and their biological activities for an effective treatment of lung cancer

in-vitro,

Lung,

A549

EPR↑, cellular uptake of the AgNPs results indicated that the AgNPs accumulated within the cell.
BAX↑, Bax, Bcl-2, caspase-3 (CASP3), caspase-9 (CASP9)
Bcl-2↑,
Casp3↑,
Casp9↑,
DNAdam↑, apoptotic effects of the AgNPs through DNA fragmentation test, flow cytometry and cell cycle analysis indicated the induction of apoptosis in the A549 cell line.
TumCCA↑,
Apoptosis↑,

4439-

AgNPs,

Anticancer Potential of Green Synthesized Silver Nanoparticles Using Extract of Nepeta deflersiana against Human Cervical Cancer Cells (HeLA)

in-vitro,

Cerv,

HeLa

33 nm

ROS↑, significant increase in ROS and lipid peroxidation (LPO), along with a decrease in MMP and glutathione (GSH) levels.
lipid-P↑,
MMP↓,
GSH↓,
TumCCA↑, significant increase in ROS and lipid peroxidation (LPO), along with a decrease in MMP and glutathione (GSH) levels.
Apoptosis↑,
Necroptosis↑,
TumCD↑, AgNPs-induced cell death in HeLA cells suggested the anticancer potential of ND-AgNPs.
Dose↝, ND-AgNPs at 10, 25, and 50 µg/ml concentration

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

4383-

AgNPs,

Exploring the Potentials of Silver Nanoparticles in Overcoming Cisplatin Resistance in Lung Adenocarcinoma: Insights from Proteomic and Xenograft Mice Studies

in-vitro,

Lung,

A549

AgNPs was 23.45 nm, with zeta potentials lying on −20.33 mV.

in-vivo,

Lung,

A549

A549 and A549/DDP-bearing mice

Apoptosis↑, Silver nanoparticles (AgNPs) have shown great potential as therapeutic agents due to their ability to cause apoptotic cell death in cancer cells.
VEGF↓, suppressing the VEGF signaling pathway, repressing p53-mediated pathways, promoting cell cycle arrest,
P53↓,
TumCCA↑,
ROS↑, we found that AgNPs induced ROS generation
AntiTum↑, AgNPs exhibit similar antitumoral effects on both A549 and A549/DDP-bearing mice.
eff↑, AgNPs are internalized by cells far more effectively than free Ag+ under identical exposure conditions
ATP↓, AgNPs exposure also decreased basal respiration (52.3 ± 4.6 pmol/min/106 cells), maximal respiration (109.2 ± 12.2 pmol/min/106 cells), ATP production (
eff↑, These results explain why AgNPs remain effective against cisplatin-resistant A549 cells.
CTR1↑, recent studies have shown that AgNPs treatment significantly upregulates CTR1

4564-

AgNPs,

GoldNP,

Cu,

Chemo,

PDT

Cytotoxicity and targeted drug delivery of green synthesized metallic nanoparticles against oral Cancer: A review

Review,

Var,

ROS↑, graphical abstract
DNAdam↑, inducing cell death through apoptotic signaling pathways, and inducing excess reactive oxygen species (ROS) in tumor cells, which leads to oxidative damage and increased production of proapoptotic enzymes
TumCCA↑,
eff↑, Metallic nanoparticles, especially those derived from metals, improve the effectiveness of anticancer agents by facilitating targeted delivery and sustained release at tumor sites.
Apoptosis↑,
eff↓, Au NPs are notable for their biocompatibility and are utilized in photothermal therapy to convert light into heat, effectively destroying cancer cells
ChemoSen↑, Magnesium oxide nanoparticles (MgO NPs) induce apoptosis through ROS production and enhance the impact of chemotherapy drugs, synthesized with plant extracts as reducing agents.

4563-

AgNPs,

Rad,

Silver nanoparticles enhance neutron radiation sensitivity in cancer cells: An in vitro study

in-vitro,

BC,

MCF-7

in-vitro,

Ovarian,

SKOV3

in-vitro,

GBM,

U87MG

in-vitro,

Melanoma,

A431

RadioS↑, Here, we, for the first time, present the results of the radiosensitizing properties of silver nanoparticles (AgNPs) (possessing low toxicity towards human body) against cancer cells under neutron irradiation.
ROS↑, The mechanism of AgNPs anticancer (intrinsic) effect includes oxidative stress, cell cycle arrest and apoptosis, activate endoplasmic reticulum stress, modulate various signaling pathways, etc
TumCCA↑,
Apoptosis↑,
ER Stress↑,

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

4558-

AgNPs,

Role of Oxidative and Nitro-Oxidative Damage in Silver Nanoparticles Cytotoxic Effect against Human Pancreatic Ductal Adenocarcinoma Cells

in-vitro,

PC,

PANC1

3.19 ug/mL

ROS↑, it is known that AgNPs may induce an accumulation of ROS and alteration of antioxidant systems in different type of tumors, and they are indicated as promising agents for cancer therapy.
selectivity↑, We found that the increase was lower in noncancer cells.
NO↑, PANC-1 cells with 0.5–5 μg/mL of 2.6 nm AgNPs or 5–100 μg/mL of 18 nm AgNPs caused an increase of NO level in a concentration-dependent manner
SOD↓, We observed a significant reduction in cytosolic and mitochondrial SOD and GPX-4 at protein level
GPx4↓,
Catalase↓, we showed that 2.6 nm AgNPs caused a higher decrease in SOD1, SOD2, and CAT at mRNA level after 24 h incubation than 18 nm AgNPs
TumCCA↑, 2.6 nm and 18 nm AgNPs, we noticed a decrease of G0/G1 phase cell population in a concentration-dependent manner compared with control
MMP↓, increase of the percentage of cells with low mitochondrial membrane potential (Δψm), compared to the untreated cells

4549-

AgNPs,

Silver nanoparticles: Synthesis, medical applications and biosafety

Review,

Var,

Review,

Diabetic,

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

4542-

AgNPs,

Silver Nanoparticles (AgNPs): Comprehensive Insights into Bio/Synthesis, Key Influencing Factors, Multifaceted Applications, and Toxicity─A 2024 Update

Review,

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.

5143-

AgNPs,

Thermal Co-reduction engineered silver nanoparticles induce oxidative cell damage in human colon cancer cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis

in-vitro,

CRC,

HCT116

28.11 μg/ml.

ROS↑, AgNP induces oxidative stress on HCT116 by increased levels of lipid peroxidation and reduced levels of glutathione.
lipid-P↑,
GSH↓,
MMP↓, Mitochondrial membrane depolarization was also analysed and Western blot analysis confirms the increased level of Bcl and Caspase-3 which indicates the mitochondrial -mediated apoptosis.
Casp3↑,
Apoptosis↑,
TumCCA↑, Mitochondrial membrane depolarization was also analysed and Western blot analysis confirms the increased level of Bcl and Caspase-3 which indicates the mitochondrial -mediated apoptosis.

334-

AgNPs,

Silver-Based Nanoparticles Induce Apoptosis in Human Colon Cancer Cells Mediated Through P53

in-vitro,

Colon,

HCT116

Bax:Bcl2↑, as demonstrated by an increase in 4´,6-diamidino-2-phenylindole-stained apoptotic nuclei, BAX/BCL-XL ratio, cleaved poly(ADP-ribose) polymerase, p53, p21 and caspases 3, 8 and 9, and by a decrease in the levels of AKT and NF-κB.
P53↑, AgNPs are bona fide anticancer agents that act in a p53-dependent manner
P21↑,
Casp3↑,
Casp8↑,
Casp9↑,
Akt↓,
NF-kB↓,
DNAdam↑, AgNPs caused DNA damage and reduced the interaction between p53 and NF-κB
TumCCA↑, The cell population in the G1 phase decreased, and the S-phase population increased after AgNP treatment

361-

AgNPs,

Annona muricata assisted biogenic synthesis of silver nanoparticles regulates cell cycle arrest in NSCLC cell lines

in-vitro,

Lung,

A549

 80 ± 6.3 nm as average size

 6 µg/ml

Apoptosis↑,
Casp↑,
TumCCA↑,

359-

AgNPs,

Anti-cancer & anti-metastasis properties of bioorganic-capped silver nanoparticles fabricated from Juniperus chinensis extract against lung cancer cells

in-vitro,

Lung,

A549

 9.87ug/ml

in-vitro,

Nor,

HEK293

111.3ug/ml

normal cells

Casp3↑,
Casp9↑,
P53↑,
ROS↑,
MMP2↓,
MMP9↓,
TumCCA↑, cessation in the G0/G1 phase
*toxicity↓, 9.87ug/ml(cancer cells) and 111.26 µg/ml(normal cells)
TumCMig↓,
TumCI↓,

356-

AgNPs,

MF,

Anticancer and antibacterial potentials induced post short-term exposure to electromagnetic field and silver nanoparticles and related pathological and genetic alterations: in vitro study

in-vitro,

BC,

MCF-7

 10 µM/ml + 1mT,2hr

 likely 50-60Hz and 1mT

in-vitro,

Bladder,

HTB-22

4uM/ml

 calculated IC50 value of AgNPs was 4.15 ± 0.20 μM/ml

Apoptosis↑,
P53↑, Up-regulation in the expression level of p53, iNOS and NF-kB genes as well as down-regulation of Bcl-2 and miRNA-125b genes were detected post treatment.
iNOS↑,
NF-kB↑,
Bcl-2↓,
ROS↑, the present study evaluated the levels of ROS as well as the antioxidant enzymes (SOD and CAT)
SOD↑,
TumCCA↑, S phase arrest and accumulation of cells in G2/M phase was observed following exposure to AgNPs and EMF, respectively.
eff↑, Apoptosis induction was obvious following exposure to either ELF-EMF or AgNPs, however their apoptotic potential was intensified when applied in combination
Catalase↑, Catalase (CAT)
other↑, swollen cells, swollen nuclei with mixed euchromatin and heterochromatin, ruptured cell membranes

358-

AgNPs,

Preparation of triangular silver nanoparticles and their biological effects in the treatment of ovarian cancer

vitro+vivo,

Ovarian,

SKOV3

 mice

TumCCA↑, arrested the cell cycle in G0/G1 phase
ROS↑,
Casp3↑,
TumCG↓,
cycD1/CCND1↓, and cyclinA2

393-

AgNPs,

Green synthesized plant-based silver nanoparticles: therapeutic prospective for anticancer and antiviral activity

in-vitro,

NA,

HCT116

mtDam↑,
ROS↑,
TumCCA↑,
Casp3↑,
BAX↑,
Bcl-2↓,
P53↑,

386-

AgNPs,

Tam,

Synergistic anticancer effects and reduced genotoxicity of silver nanoparticles and tamoxifen in breast cancer cells

in-vitro,

BC,

MCF-7

35uM(AgNP)+20uM(Tam)

in-vitro,

BC,

MDA-MB-231

P53↑,
BAX↑,
Bcl-2↓,
Casp3↑,
DNAdam↑,
TumCCA↑,

2288-

AgNPs,

Silver Nanoparticle-Mediated Cellular Responses in Various Cell Lines: An in Vitro Model

Review,

Var,

*ROS↑, Several studies have reported that AgNPs induce genotoxicity and cytotoxicity in both cancer and normal cell lines
Akt↓, high ROS levels, and reduced Akt and ERK signaling.
ERK↓,
DNAdam↑, increased ROS production, leading to oxidative DNA damage and apoptosis
Ca+2↑, The damage caused to the cell membrane is due to intracellular calcium overload, and further causes ROS overproduction and mitochondrial membrane potential variation
ROS↑,
MMP↓,
Cyt‑c↑, AgNPs induce apoptosis through release of cytochrome c into the cytosol and translocation of Bax to the mitochondria, and also cause cell cycle arrest in the G1 and S phases
TumCCA↑,
DNAdam↑, main result of AgNP toxicity is direct and oxidative DNA damage, ultimately causing apoptosis
Apoptosis↑,
P53↑, AgNPs induce apoptosis in spermatogonial stem cells through increased levels of ROS; mitochondrial dysfunction; upregulation of p53 expression; pErk1/2;
p‑ERK↑,
ER Stress↑, endoplasmic reticulum (ER) stress-induced apoptosis caused by AgNPs has attracted much research interest
cl‑ATF6↑, cleavage of activating transcription factor 6 (ATF6), and upregulation of glucose-regulated protein-78 and CCAAT/enhancer-binding protein-homologous protein (CHOP/GADD153)
GRP78/BiP↑,
CHOP↑,
UPR↑, In order to protect the cells against nanoparticle-mediated toxicity, the ER rapidly responds with the unfolded protein response (UPR), an important cellular self-protection mechanism

2836-

AgNPs,

Gluc,

Glucose capped silver nanoparticles induce cell cycle arrest in HeLa cells

in-vitro,

Cerv,

HeLa

eff↝, AgNPs synthesized are stable up to 10 days without silver and glucose dissolution.
TumCCA↑, AgNPs block the cells in S and G2/M phases, and increase the subG1 cell population.
eff↑, HeLa cells take up abundantly and rapidly AgNPs-G resulting toxic to cells in amount and incubation time dependent manner.
eff↑, The dissolution experiments demonstrated that the observed effects were due only to AgNPs-G since glucose capping prevents Ag+ release.
ROS↑, AgNPs cause toxic responses via induction of oxidative stress as consequence of the generation of intracellular (ROS), depletion of glutathione (GSH), reduction of the superoxide dismutase (SOD) enzyme activity, and increased lipid peroxidation
GSH↓,
SOD↓,
lipid-P↑,
LDH↑, significant LDH levels increase with the highest amount of AgNPs-G and maximum of toxicity was seen at 12 h.

5341-

Ajoene,

Ajoene (natural garlic compound): a new anti-leukaemia agent for AML therapy

Review,

AML,

eff↑, Ajoene (4,5,9-trithiadodeca-1,6,11-triene-9-oxide) is a garlic-derived compound produced most efficiently from pure allicin and has the advantage of a greater chemical stability than allicin.
AntiThr↑, ajoene have demonstrated its best-known anti-thrombosis, anti-microbial and cholesterol lowering activities.
Bacteria↓,
LDH↓,
TumCP↓, Ajoene was shown to inhibit proliferation and induce apoptosis of several human leukaemia CD34-negative cells including HL-60, U937, HEL and OCIM-1
TumCCA↑, Studies have shown the anti-proliferation activity of ajoene to be associated with a block in the G2/M phase of cell cycle in human myeloid leukaemia cells.
Bcl-2↓, The apoptosis inducing activity of ajoene is via the mitochondria-dependent caspase cascade through a significant reduction of the anti-apoptotic bcl-2 that results in release of cytochrome c and the activation of caspase-3.
Cyt‑c↑,
Casp3↑,

5356-

AL,

Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects

Review,

GC,

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

2647-

AL,

The Mechanism in Gastric Cancer Chemoprevention by Allicin

Review,

GC,

ChemoSen↓, Experiments have shown that allicin can be chemopreventive to gastric cancer
TumCG↓, by inhibiting the growth of cancer cells, arresting cell cycle at G2/M phase, endoplasmic reticulum (ER) stress, and mitochondria-mediated apoptosis, which includes the caspase-dependent/-independent pathways and death receptor pathway.
TumCCA↑,
ER Stress↑,
Apoptosis↑,
Casp↑,
DR5↑, DR5 (death receptor 5) was found to be upregulated following allicin treatment

2655-

AL,

Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities

Review,

GC,

TGF-β↓, Allicin can reduce the expression of TGF-2 and its receptor after entering directly into gastric cancer cell
cycD1/CCND1↓, followed by not only downexpression of cyclinD1, cyclinE, and cyclin-dependent kinase (CDK),
cycE/CCNE↓,
CDK1↓, cyclin-dependent kinase (CDK)
DNAdam↑, but also causing DNA damage and generating ROS
ROS↑,
BAX↑, Allicin increases the levels of Bax (proapoptotic protein), Bcl-2 (antiapoptotic protein), and JNK
JNK↑,
MMP↓, through reduction in outer mitochondrial membrane potential
p38↑, allicin induces p38 mitogen that could induce the protein kinase (MAPK) and then increase the expression of Fas binding to Fas ligand (Fas L) and finally activate death pathway through activation of cyt C and caspase-8.
MAPK↑,
Fas↑,
Cyt‑c↑,
Casp8↑,
PARP↑, allicin makes caspase-dependent apoptosis through elevating PARP, caspase-3 and caspase-9, which are mediated by enhanced discharging of mitochondria cyt C to the cytosol.
Casp3↑,
Casp9↑,
Ca+2↑, allicin induces apoptosis via increasing the amounts of free Ca2+, ER stress.
ER Stress↑,
P21↑, generating ROS to produce p21 and phospho-p53 (Ser15).
CDK2↓, Then p21 suppressed the CDK-4/6/cyclinD complex, P21-PCNA, P21-CDK2, and subsequently reduced cdk1/cyclinB1 complex for G2/M phase cell cycle arrest
CDK6↑,
TumCCA↑,
CDK4↓, Then p21 suppressed the CDK-4/6/cyclinD complex

2663-

AL,

Therapeutic Effect of Allicin on Glioblastoma

in-vitro,

GBM,

U251

in-vitro,

GBM,

U87MG

BioAv↝, After processing, such as cutting, crushing, chewing, or dehydration, alliinase rapidly breaks down alliin to form allicin. Allicin is immediately decomposed to other organosulfur compounds such as diallyl sulphide (DAS), diallyl disulfide(DADS), and
TumCCA↑, The results show DATS can reduce tumor growth by inhibits cell cycle progression and promotes p53-mediated tumor suppression pathways
P53↑,
HDAC↓, The findings demonstrate that DATS can inhibit U87MG cell growth in vivo by inhibiting HDAC [10].
CSCs↓, Inhibition of cancer stem cells(CSC)
ROS↑, DATS can induce apoptosis by ROS through regulation of Bcl-2 and have anticancer effect on human glioblastoma (U87MG) and neuroblastoma (SH-SY5Y) cells
ChemoSen↑, The most interesting thing is allicin can enhance the sensitivity of TMZ-resistant cells to TMZ by inhibiting MGMT expression.
MGMT↓,

2660-

AL,

Allicin: A review of its important pharmacological activities

Review,

AD,

Review,

Var,

Review,

Park,

Review,

Stroke,

*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↓,

2000-

AL,

Exploring the ROS-mediated anti-cancer potential in human triple-negative breast cancer by garlic bulb extract: A source of therapeutically active compounds

in-vitro,

BC,

MDA-MB-231

5–20 mg/mL

13.69 mg/mL

in-vitro,

BC,

MCF-7

5–20 mg/mL5–20 mg/mL

15.35 mg/mL

in-vitro,

Nor,

selectivity↑, The inhibitory effect of ASEE was more pronounced in MDA-MB-231 cells than in MCF-7 cells, however, no substantial cytotoxicity was seen in normal Vero cells.
TumCG?,
*toxicity∅, no substantial cytotoxicity was seen in normal Vero cells
ROS↑, TNBC cells treated with high concentrations of ASEE were found in the late apoptotic stage and exhibited an increase in ROS level and a reduction in MMP
MMP↓,
TumCCA↑, increased the percentage of cells in the G2/M phase
P53↑, ASEE upregulated the p53 and Bax proteins while downregulated the Bcl-2, p-Akt, and p-p38 proteins.
Bcl-2↓,
p‑Akt↓,
p‑p38↓,
*ROS∅, Vero normal cells did not display the unusual morphological alteration and reduction in cell viability. ROS production revealed a 1.21 % ROS level only in control cells that is typically seen in healthy cells.

254-

AL,

Allicin and Cancer Hallmarks

Review,

Var,

NRF2⇅, 40 nM
BAX↑,
Bcl-2↓,
Fas↑,
MMP↓,
Bax:Bcl2↑,
Cyt‑c↑,
Casp3↑,
Casp12↑,
GSH↓, Allicin can easily penetrate the cell membrane and react with the cellular thiol to transiently deplete the intracellular GSH level, inducing the inhibition of cell cycle progression and growth arrest [98].
TumCCA↑,
ROS↑, An in vitro study indicated that allicin encourages oxidative stress and autophagy in Saos-2 and U2OS (osteosarcoma cells) by modulating the MALATI-miR-376a-Wnt and β-catenin pathway [99].
antiOx↓, As an antioxidant phytochemical, it scavenges reactive oxygen species (ROS) and protects cells from oxidative DNA damage [34].

255-

AL,

Allicin induces cell cycle arrest and apoptosis of breast cancer cells in vitro via modulating the p53 pathway

in-vitro,

BC,

MCF-7

in-vitro,

BC,

MDA-MB-231

Apoptosis↑,
P53↑, through p53 activation
Casp3↑,
P53↑,
TPM4↓,
TumCCA↑, Allicin induces cell cycle arrest
THBS1↑, allicin up-regulated the mRNA and protein expression of A1BG and THBS1 while down-regulated the expression of TPM4

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.

3443-

ALA,

Molecular and Therapeutic Insights of Alpha-Lipoic Acid as a Potential Molecule for Disease Prevention

Review,

Var,

Review,

AD,

*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 (

298-

ALA,

Rad,

Synergistic Tumoricidal Effects of Alpha-Lipoic Acid and Radiotherapy on Human Breast Cancer Cells via HMGB1

in-vitro,

BC,

MDA-MB-231

Apoptosis↑,
P53↑,
p38↑,
NF-kB↑, NF-κB were significantly increased in the ALA+RT group compared to the control
TumCCA↑, G2/M cell cycle arrest.

1252-

aLinA,

α-Linolenic acid induces apoptosis, inhibits the invasion and metastasis, and arrests cell cycle in human breast cancer cells by inhibiting fatty acid synthase

in-vitro,

BC,

FASN↓, α-linolenic acid (ALA) as a novel fatty acid synthase (FASN) inhibitor
Apoptosis↑,
TumCI↓,
TumMeta↓,
TumCCA↑,

554-

Anamu,

Petiveria alliacea extracts uses multiple mechanisms to inhibit growth of human and mouse tumoral cells

in-vitro,

NA,

769-P

TumCCA↑, induce G2 cell cycle arrest
HSP70/HSPA5↓,
HSP90↓,

1158-

And,

GEM,

Andrographolide causes apoptosis via inactivation of STAT3 and Akt and potentiates antitumor activity of gemcitabine in pancreatic cancer

TumCP↓,
TumCCA↑,
Apoptosis↑,
STAT3↓,
Akt↓,
P21↑,
BAX↑,
cycD1/CCND1↓,
cycE/CCNE↓,
survivin↓,
XIAP↓,
Bcl-2↓,
eff↑, ANDRO combined with gemcitabine significantly induce stronger cell cycle arrest and more obvious apoptosis than each single treatment.

1353-

And,

Andrographolide Induces Apoptosis and Cell Cycle Arrest through Inhibition of Aberrant Hedgehog Signaling Pathway in Colon Cancer Cells

in-vitro,

Colon,

HCT116

ChemoSen↑, combination with 5FU, andrographolide exhibited synergistic effect
TumCCA↑, G2/M phase arrest
CDK1↓,
CycB/CCNB1↓,
HH↓, repressed the colon cancer cell growth via inhibiting Hh signaling pathway
Smo↓,
Gli1↓,

1354-

And,

Andrographolide induces protective autophagy and targeting DJ-1 triggers reactive oxygen species-induced cell death in pancreatic cancer

in-vitro,

PC,

0, 10, 20, 40 µM

in-vivo,

PC,

Apoptosis↑,
DJ-1↓, reduction in DJ-1 expression caused by Andro led to ROS accumulation
ROS↑,
TumAuto↑,
TumCCA↑, G2/M phase
TumCP↓,
TumW↓,
eff↓, pro-apoptotic effect of Andro was attenuated when NAC was co-administered

Showing Research Papers: 1 to 50 of 697
Page 1 of 14 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 697

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 2,
Total Targets: 188

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 3, GSH↑, 1, GSTs↑, 1, Keap1↓, 1, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, NRF2↑, 2, ROS↓, 3, ROS↑, 1, ROS∅, 1, SOD↑, 1, TBARS↓, 1,

Metal & Cofactor Biology ⓘ

IronCh↑, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, glucose↓, 1, H2S↑, 1, LDH↓, 2,

Cell Death ⓘ

Akt↓, 1, iNOS↓, 1, JNK↑, 1,

Transcription & Epigenetics ⓘ

other↑, 1,

Protein Folding & ER Stress ⓘ

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

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1,

Barriers & Transport ⓘ

BBB↑, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IFN-γ↑, 1, IL2↑, 1, IL6↓, 1, Inflam↓, 3, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1, TNF-α↑, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 1, BioAv↝, 1, eff↑, 3, Half-Life↓, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

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

Functional Outcomes ⓘ

AntiAge↑, 1, AntiDiabetic↑, 1, Bone Healing↑, 1, cardioP↓, 1, cardioP↑, 1, chemoP↑, 1, cognitive↑, 2, hepatoP↑, 1, memory↑, 2, motorD↑, 1, neuroP↑, 3, toxicity↓, 2, toxicity↝, 1, toxicity∅, 1, Wound Healing↑, 1,

Infection & Microbiome ⓘ

AntiFungal↑, 1, AntiViral↑, 2, Bacteria↓, 2,
Total Targets: 69

Scientific Paper Hit Count for: TumCCA, Tumor cell cycle arrest

33 Curcumin
30 Quercetin
29 Silver-NanoParticles
24 Thymoquinone
22 Apigenin (mainly Parsley)
22 Berberine
22 Sulforaphane (mainly Broccoli)
17 Phenethyl isothiocyanate
15 Artemisinin
15 Baicalein
15 Capsaicin
15 Piperlongumine
14 Fisetin
13 Shikonin
12 Magnetic Fields
12 Ashwagandha(Withaferin A)
12 Betulinic acid
12 Resveratrol
11 Radiotherapy/Radiation
11 EGCG (Epigallocatechin Gallate)
11 Emodin
10 Garcinol
10 Magnolol
9 Rosmarinic acid
9 Propolis -bee glue
9 Graviola
9 Honokiol
9 Lycopene
9 Silymarin (Milk Thistle) silibinin
8 Allicin (mainly Garlic)
8 Carvacrol
8 Chrysin
8 Ellagic acid
8 Luteolin
8 Urolithin
7 Chemotherapy
7 Cisplatin
7 chitosan
7 Phenylbutyrate
7 Pterostilbene
6 5-fluorouracil
6 doxorubicin
6 Astaxanthin
6 Berbamine
6 Celastrol
6 Naringin
6 Selenite (Sodium)
5 Boswellia (frankincense)
5 Chlorogenic acid
5 Paclitaxel
5 Plumbagin
5 salinomycin
5 Ursolic acid
4 Coenzyme Q10
4 Vitamin C (Ascorbic Acid)
4 Bufalin/Huachansu
4 Brucea javanica
4 Boron
4 Caffeic Acid Phenethyl Ester (CAPE)
4 Thymol-Thymus vulgaris
4 Selenium
4 HydroxyTyrosol
4 Laetrile B17 Amygdalin
4 VitK3,menadione
4 Selenium NanoParticles
4 Aflavin-3,3′-digallate
4 Vitamin K2
3 Astragalus
3 Copper and Cu NanoParticles
3 Alpha-Lipoic-Acid
3 Andrographis
3 Gemcitabine (Gemzar)
3 Biochanin A
3 borneol
3 Bruteridin(bergamot juice)
3 Caffeic acid
3 Carnosic acid
3 Date Fruit Extract
3 Piperine
3 Ferulic acid
3 Gallic acid
3 Gambogic Acid
3 Genistein (soy isoflavone)
3 Hydroxycinnamic-acid
3 Juglone
3 Metformin
3 Magnetic Field Rotating
3 Propyl gallate
2 Glucose
2 Gold NanoParticles
2 Photodynamic Therapy
2 Ascorbyl Palmitate
2 Melatonin
2 Atorvastatin
2 beta-glucans
2 Celecoxib
2 Chlorophyllin
2 Dichloroacetate
2 Deguelin
2 diet Methionine-Restricted Diet
2 Electrical Pulses
2 carboplatin
2 Hyperthermia
2 itraconazole
2 Licorice
2 Methylene blue
2 Magnesium
2 Oleuropein
2 Parthenolide
1 tamoxifen
1 Ajoene (compound of Garlic)
1 alpha Linolenic acid
1 dibenzyl trisulphide(DTS) from Anamu
1 Arctigenin
1 Aloe anthraquinones
1 immunotherapy
1 Baicalin
1 D-limonene
1 epirubicin
1 brusatol
1 Bacopa monnieri
1 Bromelain
1 Butyrate
1 Zinc
1 Carnosine
1 Selenate
1 Docetaxel
1 Chocolate
1 Vitamin E
1 Docosahexaenoic Acid
1 diet FMD Fasting Mimicking Diet
1 Disulfiram
1 Evodiamine
1 Citric Acid
1 Sorafenib (brand name Nexavar)
1 Fenbendazole
1 Shilajit/Fulvic Acid
1 Galloflavin
1 Rapamycin
1 Inositol
1 Methylglyoxal
1 Methylsulfonylmethane
1 Mushroom Chaga
1 Myricetin
1 Niclosamide (Niclocide)
1 Sanguinarine
1 Psoralidin
1 Rutin
1 Oxaliplatin
1 Sulfasalazine
1 Auranofin
1 Salvia miltiorrhiza
1 Spermidine
1 Osimertinib
1 Adagrasib

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#:322  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

TumCCA Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Metal & Cofactor Biology ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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