Bcl-2 Cancer Research Results

Bcl-2, B-cell CLL/lymphoma 2: Click to Expand ⟱

Source: HalifaxProj (inhibit) CGL-Driver Genes

Type: Antiapoptotic Oncogene

The proteins of BCL-2 family are classified into three subgroups, i.e., the anti-apoptotic/pro-survival proteins represented by BCL-2 and BCL-XL, the pro-apoptotic proteins represented by BAX and Bak, and the pro-apoptotic BH3-only proteins represented by BAD and BID.
Since the expression of Bcl-2 protein in tumor cells is much higher than that in normal cells, inhibitors targeting it have little effect on normal cells.

Scientific Papers found: Click to Expand⟱

5271-

3BP,

The anticancer agent 3-bromopyruvate: a simple but powerful molecule taken from the lab to the bedside

Review,

Var,

selectivity↑, 3-bromopyruvate (3BP), a simple alkylating chemical compound was presented to the scientific community as a potent anticancer agent, able to cause rapid toxicity to cancer cells without bystander effects on normal tissues.
selectivity↑, results obtained in cancer research with this small molecule have contradicted the just noted general fear. Indeed, a promising drug has been revealed with an effective mechanism of action and an outstanding selectivity towards cancer cells
ATP↓, once inside cancer cells 3BP can then inhibit both of their energy (ATP) producing systems, i.e., glycolysis, likely by inhibiting hexokinase-2 (hk-2) and mitochondrial oxidative phosphorylation
Glycolysis↓,
HK2↓,
mt-OXPHOS↓,
GAPDH↓, Different reports have shown that 3BP is able to inhibit GAPDH activity leading to the loss of the ATP-producing steps that occur downstream of this enzyme
mtDam↑, Mitochondria related cell death has also been reported following 3BP treatment.
GSH↓, Ehrke and co-workers have demonstrated that 3BP inhibits glycolysis and deplete the glutathione levels in primary rat astrocytes
ROS↑, Others have also observed an increase in ROS levels following 3BP treatment that induces endoplasmic reticulum stress
ER Stress↑,
TumAuto↑, Autophagy has been associated with 3BP activity in breast cancer cell lines (Zhang et al., 2014),
LC3‑Ⅱ/LC3‑Ⅰ↑, 3BP leads to aggressive autophagy involving a decrease in the ratio of LC3I/LC3II and the levels of p62 as well as dephosphorylation of Akt and p53.
p62↓,
Akt↓,
HDAC↓, 3BP’s, it has been reported to be involved in suppressing epigenetic events as it inhibits histone deacetylase (HDAC) isoforms 1 and 3 in MCF-7 breast cancer cells leading to apoptosis
TumCA↑, Proliferation inhibition by 3BP treatment has also been related with the induction of S-phase and G2/M- phase arrest (Liu et al. 2009)
Bcl-2↓, downregulation of the expression of Bcl-2, c-Myc and mutant p53, the upregulation of Bax, activation of caspase-3 and mitochondrial leakage of cytochrome c
cMyc↓,
Casp3↑,
Cyt‑c↑,
Mcl-1↓, mitochondria mediated apoptosis triggered by 3BP was found to be associated with the downregulation of Mcl-1 through the phosphoinositide-3-kinase/Akt pathway (Liu et al. 2014).
PARP↓, 3BP treatment decreases the levels of poly(ADP-ribose) polymerase (PARP) and cleaved PARP.
ChemoSen↑, it might be a good adjuvant for commonly used chemotherapy agents, or a replacement for such agents.

5277-

3BP,

3-Bromopyruvate inhibits pancreatic tumor growth by stalling glycolysis, and dismantling mitochondria in a syngeneic mouse model

in-vivo,

PC,

Panc02

mouse model

HK2↓, It exerts potent anticancer effects by inhibiting hexokinase II enzyme (HK2) of the glycolytic pathway in cancer cells while not affecting the normal cells.
selectivity↑, it doesn’t affect the normal cells but strongly toxic to cancer cells
ATP↓, 3-BP killed 95% of Panc-2 cells at 15 μM concentration and severely inhibited ATP production by disrupting the interaction between HK2 and mitochondrial Voltage Dependent Anion Channel-1 (VDAC1) protein.
mtDam↑, Electron microscopy data revealed that 3-BP severely damaged mitochondrial membrane in cancer cells.
Dose↝, We further examined therapeutic effect of 3-BP in syngeneic mouse pancreatic cancer model by treating animals with 10, 15 and 20 mg/kg dose. 3-BP at 15 & 20 mg/kg dose level significantly reduced tumor growth by approximately 75-80% in C57BL/6 female
TumCG↓, 3-BP inhibit in vivo pancreatic tumor growth in C57BL/6 mouse model
Casp3↑, observed enhanced expression of active caspase-3 in tumor tissues exhibited apoptotic death.
Glycolysis↓, Notably, metabolomic data also revealed severe inhibition in glycolysis, NADP, ATP and lactic acid production in cancer cells treated with 40 μM 3-BP.
NADPH↓,
ATP↓,
ROS↑, 3-BP treatment produces increased levels of reactive oxygen species (ROS), which causes DNA damage with reduction of free glutathione levels [11].
DNAdam↑,
GSH↓,
Bcl-2↓, Further, treatment with 40 µM of 3-BP suppressed BCL2L1 expression and causing activation of mitochondrial caspases
Casp↑,
lactateProd↓, Metabolic inhibition of glucose consumption and lactic acid production in cancer cells treated with 3-BP

5257-

3BP,

Tumor Energy Metabolism and Potential of 3-Bromopyruvate as an Inhibitor of Aerobic Glycolysis: Implications in Tumor Treatment

Review,

Var,

Glycolysis↓, In recent years, a small molecule alkylating agent, 3-bromopyruvate (3-BrPA), being an effective glycolytic inhibitor, has shown great potential as a promising antitumor drug.
mt-OXPHOS↓, Not only it targets glycolysis process, but also inhibits mitochondrial OXPHOS in tumor cells.
HK2↓, The direct inhibition of mitochondrial HK-II isolated from the rabbit liver implanted VX2 tumor via 3-BrPA was demonstrated by Ko et al. [17].
Cyt‑c↑, -BrPA treatment resulted in an increase of cytochrome c release [59,60], along with an elevated expression of active proapoptotic caspase-3 and a decrease of antiapoptotic Bcl-2 and Mcl-1 [59]
Casp3↓,
Bcl-2↓,
Mcl-1↓,
GAPDH↓, Additionally, GAPDH was found to be inhibited by 3-BrPA in several studies
LDH↓, Recent reports showed 3-BrPA had ability to inhibit post glycolysis targets and other metabolic pathways, such as LDH, PDH, TCA cycle, and glutaminolysis
PDH↓, 3-BrPA was proven to be an inhibitor of PDH [72,73,74],
TCA↓,
GlutaM↓, this inhibition of TCA cycle can lead to the impairment of glutaminolysis due to α-KG generated from glutamine is incorporated into the TCA cycle by IDH and αKD activities
GSH↓, Indeed, a remarkable decrease of reduced glutathione (GSH) level was observed after 3-BrPA treatment in both microorganisms and various tumor cells [53,61,65].
ATP↓, 3-BrPA successfully killed AS-30D hepatocellular carcinoma (HCC) cells via the inhibition of both ATP-producing glycolysis and mitochondrial respiration [17].
mitResp↓,
ROS↑, the increase of ROS and concomitant decrease of GSH were commonly found in 3-BrPA-mediated antitumor studies [53,59,61,64,65,76,77,86,89].
ChemoSen↑, When 3-BrPA was combined with cisplatin or oxaliplatin with non-toxic low-dose, 3-BrPA strikingly enhanced the antiproliferative effects of both platinum drugs in HCT116 cells and resistant p53-deficient HCT116 cells [89].
toxicity↝, Finally, two years after the first diagnosis, the patient died due to an overload of liver function rather than the tumor itself [118].

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.

Aco,

Acoschimperoside P, 2'-acetate: a Hedgehog signaling inhibitory constituent from Vallaris glabra

in-vitro,

PC,

PANC1

 0.75–6uM

in-vitro,

Pca,

DU145

HH↓, Compound 1 was active in the assay for Hedgehog signaling inhibition.
PTCH1↓, The expression of GLI-related proteins (PTCH and BCL-2) in a dose-dependent manner was also inhibited by 1.
Bcl-2↓,
Gli1↓,

1338-

AG,

The Modulatory Properties of Astragalus membranaceus Treatment on Triple-Negative Breast Cancer: An Integrated Pharmacological Method

in-vitro,

BC,

TumCI↓,
Apoptosis↑,
Symptoms↓,
PIK3CA↓,
Akt↓,
Bcl-2↓,

1295-

AG,

Cisplatin,

Chemosensitizing Effect of Astragalus Polysaccharides on Nasopharyngeal Carcinoma Cells by Inducing Apoptosis and Modulating Expression of Bax/Bcl-2 Ratio and Caspases

in-vivo,

Laryn,

mice

AntiTum↑,
Apoptosis↑,
Bcl-2↓,
BAX↑,
Casp3↑,
Casp9↑,
Bax:Bcl2↑, ratio of Bax to Bcl-2 was significantly enhanced by the APS to cisplatin

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

5436-

AG,

Therapeutic Effect of Astragalus Polysaccharides on Hepatocellular Carcinoma H22-Bearing Mice

in-vivo,

HCC,

HCC H22-bearing mice

TumCG↓, APS inhibited the growth of H22 cells with a tumor inhibition rate in the APS 400 mg·kg−1 group of 59.01%
BAX↑, APS increased Bax protein expression and decreased Bcl-2 protein expression; these proteins are apoptosis-regulating factors responsible for cell death or survival.
Bcl-2↓,
IL2↑, These results indicated that APS promotes the expression of IL-2, IL-6, and TNF-α as an H22 tumor treatment mechanism
IL6↑,
TNF-α↑,
toxicity↓, APS could inhibit H22 tumor with low toxicity.

5238-

AgNPs,

β-Sitosterol-assisted silver nanoparticles activates Nrf2 and triggers mitochondrial apoptosis via oxidative stress in human hepatocellular cancer cell line

in-vitro,

HCC,

HepG2

TumCP↓, BSS-SNPs significantly inhibited the proliferation and induced ROS and Nrf-2 expression in HepG2 cells.
ROS↑,
NRF2↑,
BAX↑, BSS-SNPs treatment caused apoptosis-related morphological changes and upregulated the pro-apoptotic markers such as bax, p53, cytochrome c, and caspases-9, -3 and downregulated bcl-2 expressions.
P53↑,
Cyt‑c↑,
Casp9↑,
Casp3↑,
Bcl-2↓,

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↑,

4416-

AgNPs,

Efficacy of curcumin-synthesized silver nanoparticles on MCF-7 breast cancer cells

in-vitro,

BC,

MCF-7

TumCMig↓, Our results showed that C-AgNPs significantly inhibited MCF-7 cell migration
Apoptosis↑, gene expression analysis indicated the induction of apoptosis by upregulation of pro-apoptotic genes BAX and P53 and downregulation of Bcl-2.
BAX↑,
P53↑,
Bcl-2↓,

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

29.3 ± 5.6 nm

 48.23 µg/ml

SDT was performed using an US frequency of 1 MHz, intensity of 2 W/cm2, and a distance of 2 cm.

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.

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.

4430-

AgNPs,

Evaluation of the Genotoxic and Oxidative Damage Potential of Silver Nanoparticles in Human NCM460 and HCT116 Cells

in-vitro,

Colon,

HCT116

20 nm

in-vitro,

Nor,

NCM460

*Bacteria↓, Nano Ag has excellent antibacterial properties and is widely used in various antibacterial materials, such as antibacterial medicine and medical devices, food packaging materials and antibacterial textiles
ROS↑, intracellular reactive oxygen species (ROS) increased
p‑p38↑, Ag NPs can promote the increase in P38 protein phosphorylation levels in two colon cells and promote the expression of P53 and Bax.
BAX↑,
Bcl-2↓, Ag NPs can promote the down-regulation of Bcl-2, leading to an increased Bax/Bcl-2 ratio and activation of P21, further accelerating cell death
BAX↑,
P21↑,
TumCD↑,
toxicity↝, low concentration of nano Ag has no obvious toxic effect on colon cells, while nano Ag with concentrations higher than 15 μg/mL will cause oxidative damage to colon cells.

343-

AgNPs,

Silver nanoparticles of different sizes induce a mixed type of programmed cell death in human pancreatic ductal adenocarcinoma

in-vitro,

PC,

PANC1

 3.19 or 1.67 ug/mL

BAX↑,
Bcl-2↓,
P53↑,
TumAuto↑,

335-

AgNPs,

PDT,

Biogenic Silver Nanoparticles for Targeted Cancer Therapy and Enhancing Photodynamic Therapy

Review,

NA,

ROS↑,
GSH↓,
GPx↑,
Catalase↓,
SOD↓,
p38↑,
BAX↑,
Bcl-2↓,

324-

AgNPs,

CPT,

Silver Nanoparticles Potentiates Cytotoxicity and Apoptotic Potential of Camptothecin in Human Cervical Cancer Cells

in-vitro,

Cerv,

HeLa

ROS↑,
Casp3↑,
Casp9↑,
Casp6↑,
GSH↓,
SOD↓,
GPx↓,
MMP↓, loss of
P53↑,
P21↑,
Cyt‑c↑,
BID↑,
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Akt↓,
Raf↓,
ERK↓,
MAP2K1/MEK1↓,
JNK↑,
p38↑,

369-

AgNPs,

Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis

in-vitro,

Liver,

ROS↑,
GSH↓,
DNAdam↑,
lipid-P↝, damage
Apoptosis↑,
BAX↑,
Bcl-2↓,
MMP↓, disruption
Casp9↑,
Casp3↑,
JNK↑,

363-

AgNPs,

Silver nanoparticles induce oxidative cell damage in human liver cells through inhibition of reduced glutathione and induction of mitochondria-involved apoptosis

ROS↑,
lipid-P↑, lipid membrane peroxidation
Apoptosis↑,
BAX↑,
Bcl-2↓,
MMP↓, disruption
Cyt‑c↑, release from mitochondria
Casp3↑,
Casp9↑,
JNK↑,

350-

AgNPs,

Cytotoxic and Apoptotic Effects of Green Synthesized Silver Nanoparticles via Reactive Oxygen Species-Mediated Mitochondrial Pathway in Human Breast Cancer Cells

in-vitro,

BC,

MCF-7

 40ug/mL

ROS↑,
MMP↓,
P53↑,
BAX↑,
Casp3↑,
Casp9↑,
Bcl-2↓,

351-

AgNPs,

Study of antitumor activity in breast cell lines using silver nanoparticles produced by yeast

in-vitro,

BC,

MCF-7

 5ug/mL

in-vitro,

BC,

T47D

Casp9↑,
Casp3↑,
Casp7↑,
Bcl-2↓,

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

402-

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+EMF(1mT)

4.15 μM/ml for AgNPs

P53↑,
iNOS↑,
NF-kB↑,
Bcl-2↓,
miR-125b↓,
ROS↑, 2.9x for 2hr
SOD↑, 2.4x for 2hr

398-

AgNPs,

Bcl-2_pathway_fibrosis_via_TGF-ba-SMA_upregulation_in_rats">Silver nanoparticles induced testicular damage targeting NQO1 and APE1 dysregulation, apoptosis via Bax/Bcl-2 pathway, fibrosis via TGF-β/α-SMA upregulation in rats

in-vivo,

Testi,

rats

Bcl-2↓,
Casp3↑,
GSH↓,
MDA↑,
NO↑,
H2O2↑,
SOD↓,

397-

AgNPs,

GEM,

Silver nanoparticles enhance the apoptotic potential of gemcitabine in human ovarian cancer cells: combination therapy for effective cancer treatment

in-vitro,

Ovarian,

A2780S

50 nM GEM, 50 nM AgNPs

6nm

P53↑,
P21↑,
BAX↑,
Bak↑,
Cyt‑c↑,
Casp3↑,
Casp9↑,
Bcl-2↓,
ROS↑,
MMP↓,

396-

AgNPs,

Systemic Evaluation of Mechanism of Cytotoxicity in Human Colon Cancer HCT-116 Cells of Silver Nanoparticles Synthesized Using Marine Algae Ulva lactuca Extract

in-vitro,

Colon,

HCT116

P53↑,
BAX↑,
P21↑,
Bcl-2↓,

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↑,

379-

AgNPs,

Effects of green-synthesized silver nanoparticles on lung cancer cells in vitro and grown as xenograft tumors in vivo

in-vivo,

Lung,

H1299

 10ug/g of body wgt

 scid mouse

NF-kB↓,
Bcl-2↓,
Casp3↑,
survivin↑,
TumCG↓, suppressed tumor growth

381-

AgNPs,

Silver Nanoparticles Exert Apoptotic Activity in Bladder Cancer 5637 Cells Through Alteration of Bax/Bcl-2 Genes Expression

in-vitro,

Bladder,

5637

 51.12 µg/mL

 more toxic with smaller NPs (this was 30nm)

ROS↑,
BAX↑,
Bcl-2↓,
Casp3↑,
Casp7↑,
Apoptosis↑,

382-

AgNPs,

Investigation the apoptotic effect of silver nanoparticles (Ag-NPs) on MDA-MB 231 breast cancer epithelial cells via signaling pathways

in-vitro,

BC,

MDA-MB-231

Apoptosis↑,
BAX↑,
Bcl-2↓,
P53↑,
PTEN↑,
hTERT/TERT↓,
p‑ERK↓, p-ERK/Total ERK
cycD1/CCND1↓,

385-

AgNPs,

Probiotic-derived silver nanoparticles target mTOR/MMP-9/BCL-2/dependent AMPK activation for hepatic cancer treatment

in-vitro,

Hepat,

HepG2

4.217 µg/ml

in-vitro,

Hepat,

WI38

154.1 µg/ml

 healthy cells

TNF-α↑, AgNPs induce an upregulation in the synthesis of inflammation-associated cytokines, including (TNF-α and IL-33), within HepG2 cells.
IL33↑,
mTOR↓,
MMP9↓,
Bcl-2↓,
ROS↑,
Apoptosis↑,

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↑,

388-

AgNPs,

Apoptotic efficacy of multifaceted biosynthesized silver nanoparticles on human adenocarcinoma cells

in-vitro,

BC,

MCF-7

 5 and 10 µg/mL

ROS↑, ROS production
Casp3↑,
BAX↑,
P53↑,
Casp↑, Upregulation of caspases, apoptotic mediators, were observed after exposure of MCF-7 to the RAgNPs
Cyt‑c↑, The release of cytochrome c was determined after 24 h RAgNPs treatment.
MMP↓, The treated cells increased the depolarized mitochondrial membrane and decreased the polarized membranes.
DNAdam↑, Ag NPs perform well as cancer therapeutics because they can disrupt the mitochondrial respiratory chain, which induces the ROS generation, DNA damage and ATP synthesis
Bcl-2↓, Upon treatment with AgNPs or cisplatin, MCF-7 cells showed decreased Bcl-2 expression and increased Bax expression, representing the mitochondrial connection in cell death
BAX↑,

384-

AgNPs,

Dual functions of silver nanoparticles in F9 teratocarcinoma stem cells, a suitable model for evaluating cytotoxicity- and differentiation-mediated cancer therapy

in-vitro,

Testi,

LDH↓, When the cells were treated with AgNPs and AgNO3, the amount of LDH leaked into the media increased in a dose-dependent manner
ROS↑,
mtDam↑,
DNAdam↑,
P53↑,
P21↑,
BAX↑,
Casp3↑,
Bcl-2↓,
Casp9↑,
Nanog↓,
OCT4↓,

2287-

AgNPs,

Silver nanoparticles induce endothelial cytotoxicity through ROS-mediated mitochondria-lysosome damage and autophagy perturbation: The protective role of N-acetylcysteine

in-vitro,

Nor,

HUVECs

*TumCP↓, AgNPs affects the morphology and function of endothelial cells which manifests as decreased cell proliferation, migration, and angiogenesis ability
*ROS↑, AgNPs can induce excessive cellular production of reactive oxygen species (ROS), leading to damage to cellular sub-organs such as mitochondria and lysosomes
*eff↓, treatment with ROS scavenger-NAC can effectively suppress AgNP-induced endothelial damage.
*MDA↑, exposure to AgNPs increased MDA levels and decreased GSH levels.
*GSH↓,
*MMP↓, significantly reduced both MMP and ATP levels (Fig. 7) in HUVECs,
*ATP↓,
*LC3II↑, expression levels of LC3-II and p62 were significantly increase
*p62↑,
*Bcl-2↓, the anti-apoptotic protein expression level of Bcl-2 in HUVECs decreased, while the pro-apoptotic protein expression levels of Bax and Caspase-3 increased significantly.
*BAX↑,
*Casp3↑,

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↑,

5342-

Ajoene,

The garlic-derived organosulfur component ajoene decreases basal cell carcinoma tumor size by inducing apoptosis

in-vivo,

BCC,

TumVol↓, We applied ajoene topically to the tumors of 21 patients with either nodular or superficial basal cell carcinoma (BCC). A reduction in tumor size was seen in 17 patients.
Bcl-2↓, Bcl-2 expression in a selection of these tumors before and after treatment showed a significant decrease in this apoptosis-suppressing protein.
Apoptosis↑, we conclude that ajoene can reduce BCC tumor size, mainly by inducing the mitochondria-dependent route of apoptosis.

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

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↓,

1290-

AL,

Bcl-2_and_Bax_protein_in_LM-8_cells">Effect of allicin on the expression of Bcl-2 and Bax protein in LM-8 cells

in-vitro,

OS,

LM8

5.0, 10.0 and 15.0 mg/L) for 24, 48 and 72

Bcl-2↓,
BAX↑,
Apoptosis↑,
TumCG↓,

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.

245-

AL,

Allicin: a promising modulator of apoptosis and survival signaling in cancer

Review,

Var,

Fas↑,
Bcl-2↓,
BAX↑,
PI3k/Akt/mTOR↝, Allicin can inhibit excessive autophagy by activating the PI3K/Akt/mTOR and MAPK/ERK/mTOR signaling pathways.
Casp3↑,
Casp8↑,
Casp9↑,
Apoptosis↓,
*toxicity↓, Allicin-loaded nano-formulations efficiently induce apoptosis in cancer cells while minimizing toxicity to normal cells
Cyt‑c↑, allicin induces the release of cytochrome c from the mitochondria

248-

AL,

Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway

in-vitro,

GBM,

U87MG

Bcl-2↓,
BAX↑,
MAPK↑,
ERK↑,
ROS↑, antioxidant prevented inhibitory effect
p38↑,
JNK↑,

249-

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

  0.1, 1 and 10 μg/ml

Casp3↑,
p38↑,
BAX↑, up one fold
Bcl-2↓, down 35%
p38↑,
MAPK↑,

250-

AL,

Allicin Induces p53-Mediated Autophagy in Hep G2 Human Liver Cancer Cells

in-vitro,

Liver,

HepG2

 35uM

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

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].

235-

AL,

Allicin inhibits cell growth and induces apoptosis in U87MG human glioblastoma cells through an ERK-dependent pathway

in-vitro,

GBM,

U87MG

 90 μM

Apoptosis↑,
Bcl-2↓,
BAX↑,
MAPK↑, mechanisms involved in apoptosis include the mitochondrial pathway, activation of mitogen-activated protein kinases (MAPKs), and caspase cascade and oxidant enzyme system.
p‑ERK↑, In the present study, the level of ERK phosphorylation was increased
ROS↑, ROS are related to allicin-induced apoptosis in the U87MG cells.
eff↓, This study demonstrated that allicin-induced apoptosis was down-regulated by the antioxidant enzyme system

234-

AL,

Allicin Induces Anti-human Liver Cancer Cells through the p53 Gene Modulating Apoptosis and Autophagy

in-vitro,

HCC,

Hep3B

 0, 15, 20, 25, 35, 40 and 50 Î¼M of allicin for 24 h

 35 uM @24h

ROS↑, increased the production of ROS levels at 1, 3, 6 h. I
*toxicity∅, In other study, allicin treatment did not increase the leakage of lactate-dehydrogenase (LDH) of primary rat hepatocytes until 1 mM allicin treated with rat hepatocytes24. For this reason, allicin could be inferred as safe to normal liver cells
MMP↓, Allicin decreased mitochondrial membrane potential
BAX↑,
Bcl-2↓,
AIF↑,
Casp3↑, protein expression levels of caspase-3, -8, -9 increased after allicin treatment
Casp8↑,
Casp9↑,
eff↓, Allicin significantly induced ROS overproduction, whereas NAC pretreatment decreased the ROS induction by allicin exposure in Hep 3B cells
γH2AX↑, significant increase in the expression of γ-H2AX was observed at the initial stages (3, 6 h), but not at the later stages of 12, 24, 48 h
selectivity↑, data suggested that allicin induced apoptosis in p53-deficiency human liver carcinoma cells but caused autophagy in p53-normal function human liver carcinoma cells.
DNA-PK↑, increases production of ROS, triggers DNA damage

Showing Research Papers: 1 to 50 of 476
Page 1 of 10 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 476

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 195

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

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

Mitochondria & Bioenergetics ⓘ

ATP↓, 1, MMP↓, 1,

Core Metabolism/Glycolysis ⓘ

ALAT↓, 1, H2S↑, 1, LDH↓, 2,

Cell Death ⓘ

Akt↓, 1, BAX↑, 1, Bcl-2↓, 1, Casp3↑, 1, iNOS↓, 1,

Transcription & Epigenetics ⓘ

other↑, 1,

Autophagy & Lysosomes ⓘ

LC3II↑, 1, p62↑, 1,

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,

Migration ⓘ

TumCP↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 1,

Barriers & Transport ⓘ

BBB↑, 1,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL6↓, 1, Inflam↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 1,

Drug Metabolism & Resistance ⓘ

eff↓, 1, eff↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

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

Functional Outcomes ⓘ

cardioP↑, 1, chemoP↑, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 2, toxicity↓, 1, toxicity∅, 2,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 57

Scientific Paper Hit Count for: Bcl-2, B-cell CLL/lymphoma 2

31 Curcumin
28 Silver-NanoParticles
26 Thymoquinone
22 Quercetin
15 Apigenin (mainly Parsley)
14 Baicalein
13 EGCG (Epigallocatechin Gallate)
12 Allicin (mainly Garlic)
12 Betulinic acid
11 Berberine
10 Sulforaphane (mainly Broccoli)
9 Resveratrol
9 Fisetin
9 Garcinol
9 Silymarin (Milk Thistle) silibinin
8 Honokiol
8 Luteolin
8 Shikonin
7 Capsaicin
7 Carvacrol
7 Graviola
7 Piperlongumine
6 Cisplatin
6 Ashwagandha(Withaferin A)
6 Boron
6 Emodin
6 Gambogic Acid
6 Magnolol
5 5-fluorouracil
5 Astragalus
5 Magnetic Fields
5 Paclitaxel
5 Astaxanthin
5 Carnosic acid
5 Lycopene
5 Phenethyl isothiocyanate
5 Ursolic acid
4 Photodynamic Therapy
4 Alpha-Lipoic-Acid
4 Artemisinin
4 Melatonin
4 Aloe anthraquinones
4 Radiotherapy/Radiation
4 Boswellia (frankincense)
4 Ellagic acid
4 Juglone
4 Propolis -bee glue
4 Rosmarinic acid
4 Urolithin
3 3-bromopyruvate
3 Metformin
3 Berbamine
3 Chemotherapy
3 Caffeic acid
3 Chlorogenic acid
3 chitosan
3 Ferulic acid
3 Laetrile B17 Amygdalin
3 Nimbolide
3 Oleuropein
3 Phenylbutyrate
3 VitK3,menadione
2 Gemcitabine (Gemzar)
2 tamoxifen
2 Ajoene (compound of Garlic)
2 Andrographis
2 immunotherapy
2 beta-glucans
2 Baicalin
2 doxorubicin
2 Biochanin A
2 Bufalin/Huachansu
2 Brucea javanica
2 brusatol
2 Bromelain
2 borneol
2 Genistein (soy isoflavone)
2 Butyrate
2 Thymol-Thymus vulgaris
2 Chlorophyllin
2 Chrysin
2 Citric Acid
2 Docetaxel
2 HydroxyTyrosol
2 Propyl gallate
2 salinomycin
2 Selenium
2 Selenite (Sodium)
2 Vitamin K2
1 Coenzyme Q10
1 Acoschimperoside P, 2’-acetate
1 SonoDynamic Therapy UltraSound
1 Camptothecin
1 alpha Linolenic acid
1 Aspirin -acetylsalicylic acid
1 Ascorbyl Palmitate
1 Trastuzumab
1 Atorvastatin
1 D-limonene
1 epirubicin
1 selenomethionine
1 Zinc
1 Celastrol
1 Prebiotic
1 Cinnamon
1 Copper and Cu NanoParticles
1 Oxaliplatin
1 Dichloroacetophenone(2,2-)
1 Dichloroacetate
1 Date Fruit Extract
1 Evodiamine
1 Electrical Pulses
1 Gallic acid
1 carboplatin
1 Galloflavin
1 γ-linolenic acid (Borage Oil)
1 Gold NanoParticles
1 HydroxyCitric Acid
1 Hyperthermia
1 Licorice
1 Methylene blue
1 Magnetic Field Rotating
1 Methylglyoxal
1 Mushroom Shiitake, AHCC
1 Naringin
1 Oleocanthal
1 Orlistat
1 sericin
1 Physalin F & B
1 Piperine
1 Plumbagin
1 Psoralidin
1 Parthenolide
1 Pterostilbene
1 isoflavones
1 Sanguinarine
1 Scoulerine
1 polyethylene glycol
1 Selenium NanoParticles
1 Salvia miltiorrhiza
1 Spermidine
1 Aflavin-3,3′-digallate
1 Tomatine
1 Vitamin D3
1 Zerumbone

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:27  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

Bcl-2 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 ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Home Page