TumCD Cancer Research Results

TumCD, Tumor Cell Death: Click to Expand ⟱

Source:

Type:

Tumor Cell Death

Scientific Papers found: Click to Expand⟱

2325-

2DG,

Research Progress of Warburg Effect in Hepatocellular Carcinoma

Review,

Var,

HK2↓, 2-Deoxyglucose (2-DG) is a widely studied HK2 inhibitor that has been reported to inhibit glycolysis by inhibiting hexokinase
Glycolysis↓,
PKM2↓, In rat HCC models, 2-DG was shown to reduce PKM2 and LDHA expression, leading to decreased aerobic glycolysis and tumor cell death
LDHA↓,
TumCD↑,
ChemoSen↑, Combining 2-DG with sorafenib demonstrated superior antitumor effects compared to sorafenib alone, suggesting its potential for synergistic action with other anticancer drugs
eff↑, Moreover, DHA combined with 2-DG can reportedly induce apoptosis in A549 and PC-9 cells

5278-

3BP,

The effect of 3-bromopyruvate on human colorectal cancer cells is dependent on glucose concentration but not hexokinase II expression

in-vitro,

CRC,

HCT116

in-vitro,

CRC,

Caco-2

in-vitro,

CRC,

SW48

ATP↓, 3-Bromopyruvate (3BP) is a pyruvate analogue with alkylating properties that depletes cellular ATP levels and induces rapid cell death in neoplastic cells with limited cytotoxic effects against normal cells.
TumCD↑,
selectivity↑,
toxicity↓, 3BP treatment led to eradication of tumours of hepatocellular carcinoma cell origin in rats without apparent cytotoxic effects [19]
OS↑, first human case report suggested that 3BP was able to prolong survival in a cancer patient diagnosed with hepatocellular carcinoma in 2012 [19,20].
HK2?, 3BP is able to dissociate and inhibit mitochondrial HKII function, thereby reducing ATP production. 3BP binding also frees up binding sites previously occupied by HKII
Cyt‑c↑, llowing pro-apoptotic molecules (such as BAX and BAD) to promote the release of cytochrome c into the cytosol and induce eventual cell death
eff↑, Raji lymphoma cells grown under hypoxic conditions were more sensitive to 3BP than in normoxia
p‑Akt↑, 3BP induces rapid AKT phosphorylation at residue Thr-308

5259-

3BP,

Advanced cancers: eradication in all cases using 3-bromopyruvate therapy to deplete ATP

in-vivo,

HCC,

highly glycolytic cancers.  young rats. Advanced cancers (2-3cm) developed

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

5471-

AF,

Anti-Tumoral Treatment with Thioredoxin Reductase 1 Inhibitor Auranofin Fosters Regulatory T Cell and B16F10 Expansion in Mice

vitro+vivo,

Melanoma,

B16-F10

TrxR1↓, Auranofin, an FDA-approved antirheumatic drug and thioredoxin reductase 1 (TXNRD1) inhibitor, has demonstrated anti-tumoral properties
AntiTum↑,
ROS↑, TXNRD1 Inhibitors Elevated ROS Levels, Activate NRF2, and Kill B16F10 Cells In Vitro
NRF2↑,
TumCD↑,

4402-

AgNPs,

Enhancement of Triple-Negative Breast Cancer-Specific Induction of Cell Death by Silver Nanoparticles by Combined Treatment with Proteotoxic Stress Response Inhibitors

in-vitro,

BC,

BT549

in-vitro,

BC,

MDA-MB-231

in-vitro,

Nor,

MCF10

TumCD↑, Our findings provide additional support for proteotoxic stress as a mechanism by which AgNPs selectively kill TNBCs
selectivity↑,
*toxicity↝, Failure to separate dissolved silver cations (Ag+) from AgNPs before toxicity testing likely contributes to the lack of a definitive answer. Ag+ is highly toxic and has a distinct cytotoxic mechanism of action compared to AgNPs;
Dose↝, doses in the range of 4–6 mg/kg delivered systemically for multiple weeks induced therapeutic responses
OS↑, 40 patients were injected intravenously with 1.8 mg of AgNPs for 3 consecutive days (combined with standard COVID-19 treatments), and the group receiving AgNPs had significantly greater survival rate

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.

4361-

AgNPs,

GoldNP,

Biocompatible silver, gold and silver/gold alloy nanoparticles for enhanced cancer therapy: in vitro and in vivo perspectives

in-vivo,

Liver,

HepG2

IC50 values of the AgNPs, AuNPs and Ag/AuNPs on HepG2 cells were determined as 38.42 μg ml-1, 43.25 μg ml-1 and 39.20 μg ml-1

Sprague Dawley (SD) rat model

TumCD↑, IC50 values of the AgNPs, AuNPs and Ag/AuNPs on HepG2 cells were determined as 38.42 μg ml-1, 43.25 μg ml-1 and 39.20 μg ml-1
TumVol↓, tumour reduction (∼45 to 65%) was observed in the nanoparticle-treated animal
*toxicity↝, The No-Observed-Adverse-Effect-Level (NOAEL) for the AgNPs was determined to be 2000 mg per kg of body weight (bw) from an acute toxicity test.
hepatoP↑, (Ag/AuNPs) for hepatoprotective activity against diethylnitrosamine (DEN)-induced liver cancer in a Sprague Dawley (SD) rat model

4358-

AgNPs,

HPT,

Rad,

Silver nanocrystals mediated combination therapy of radiation with magnetic hyperthermia on glioma cells

in-vitro,

GBM,

U251

10 nm silver nanoparticles (AgNPs) on human glioma U251 c

RadioS↑, AgNPs showed both radio and thermo sensitivity on U251 cells from the surviving fraction curve.
eff↑, both X-rays and heat could enhance the content of cells uptake of AgNPs.
TumCD↑, potential application in enhancing effect of RT with MHT combination therapy induced killing of cancer 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.

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

4364-

AgNPs,

Selective cytotoxicity of green synthesized silver nanoparticles against the MCF-7 tumor cell line and their enhanced antioxidant and antimicrobial properties

in-vitro,

BC,

MCF-7

31.4 nm with a Zeta potential of −33.8 mV,

TumCD↑, AgNPs and the extract exhibited 70% and 40% cytotoxicity against MCF-7 cancerous cells, respectively, while CSN caused 56% cell death (at the concentration of 60 µg/mL)
selectivity↑, It was observed that AgNPs were much less cytotoxic when tested against a noncancerous cell line (L-929)
*antiOx↑, These include antioxidant, antifungal, anti-inflammatory, antiviral, anti-angiogenesis, and antimicrobial effects
*Inflam↓,
AntiTum↑, antitumor properties of AgNPs
ROS↑, AgNPs interact with mitochondria and disrupt the cellular electron transfer chain function leading to an increase in the ROS level. oxidative stress generated by ROS could be considered as a main toxicity mechanism of AgNPs against cells

4379-

AgNPs,

Exposure to silver nanoparticles induces size- and dose-dependent oxidative stress and cytotoxicity in human colon carcinoma cells

in-vitro,

CRC,

LoVo

eff↑, uptake of silver nanoparticles in cells of the human intestinal LoVo cell line was dependent on size.
TumCD↑, Silver nanoparticles in sizes of 10–100 nm induced cytotoxicity in a size- and dose-dependent manner via ROS generation.
ROS↑,
Bacteria↓, antimicrobial properties of silver nanoparticles (AgNPs)

4374-

AgNPs,

Enhancing antitumor activity of silver nanoparticles by modification with cell-penetrating peptides

in-vitro,

BC,

MCF-7

eff↑, Peptides-modified AgNPs showed significant enhancement in killing tumor cells by increasing the uptake of AgNP into cell lines
TumCD↑,

4373-

AgNPs,

In vitro toxicity of silver nanoparticles at noncytotoxic doses to HepG2 human hepatoma cells

in-vitro,

Liver,

HepG2

TumCD↑, both "nanosized particle of Ag" as well as "ionic Ag+" contribute to the toxic effects of Ag-NPs.

4372-

AgNPs,

Negligible particle-specific toxicity mechanism of silver nanoparticles: the role of Ag+ ion release in the cytosol

in-vitro,

Cerv,

HeLa

in-vitro,

Lung,

A549

TumCD↑, Cell death following the application of AgNPs is dose-dependent, and it is mostly due to Ag+ ions.

4661-

AgNPs,

Silver nanoparticles induces apoptosis of cancer stem cells in head and neck cancer

in-vitro,

HNSCC,

TumCD↑, The results showed that synthesized AgNPs have cytotoxic activity on all cancer cell lines tested with the IC50 value of a wide range (1.5–49.21 µg/ml for cell lines and 0.0643–0.1211 µg/ml for splenocytes and thymocytes).
CSCs↝, CSCs Cal33 showed higher resistance to AgNP treatment and arrest in G1/G0 phase upon cell cycle analysis.

341-

AgNPs,

Bioprospecting a native silver-resistant Bacillus safensis strain for green synthesis and subsequent antibacterial and anticancer activities of silver nanoparticles

in-vitro,

Liver,

HepG2

TumCD↑, viability of the cancer HepG2 cell line was 84.42, 65.25, 48.76 and 36.25%, respectively, at 5, 10, 15 and 20 µg mL−1 AgNPs concentrations
ROS↑,

340-

AgNPs,

Screening bioactivities of Caesalpinia pulcherrima L. swartz and cytotoxicity of extract synthesized silver nanoparticles on HCT116 cell line

in-vitro,

CRC,

HCT116

 18ug

TumCD↑, cytotoxicity effect of 77.5%

339-

AgNPs,

Cancer cell specific cytotoxic potential of the silver nanoparticles synthesized using the endophytic fungus, Penicillium citrinum CGJ-C2

in-vitro,

BC,

MCF-7

in-vitro,

Melanoma,

A431

in-vitro,

HCC,

HepG2

TumCD↑, concentration-dependent cytotoxicity

338-

AgNPs,

Biogenic silver nanoparticles: In vitro and in vivo antitumor activity in bladder cancer

vitro+vivo,

Bladder,

5637

 mice

TumCD↑, 57% tumor regression
Apoptosis↑,
TumCMig↓,
TumCP↓,

365-

AgNPs,

Silver nanoparticles affect glucose metabolism in hepatoma cells through production of reactive oxygen species

in-vitro,

Hepat,

HepG2

 0.5–7.5 µg/mL 5 nm

ROS↑,
GlucoseCon↓,
TumCD↑,
NRF2↓, Decreased mRNA levels of Nrf2

364-

AgNPs,

Differential Action of Silver Nanoparticles on ABCB1 (MDR1) and ABCC1 (MRP1) Activity in Mammalian Cell Lines

in-vitro,

Lung,

A549

 202ug/cm3

 most resistant

in-vitro,

Hepat,

HepG2

 15.8ug/cm3

 Decreased mRNA expression of most ABC transporters (not ABCB1)

in-vitro,

CRC,

SW-620

 39.4ug/cm3

 Increased mRNA expression of most ABC transporters (not ABCB1)

TumCD↑,

352-

AgNPs,

Synthesis of silver nanoparticles (Ag NPs) for anticancer activities (MCF 7 breast and A549 lung cell lines) of the crude extract of Syzygium aromaticum

in-vitro,

BC,

MCF-7

TumCD↑, significant anticancer activity

354-

AgNPs,

Silver nanoparticles induce SH-SY5Y cell apoptosis via endoplasmic reticulum- and mitochondrial pathways that lengthen endoplasmic reticulum-mitochondria contact sites and alter inositol-3-phosphate receptor function

in-vitro,

neuroblastoma,

SH-SY5Y

  Ca2+ overload and disrupted homeostasis in the mitochondria triggered apoptotic cell death.

TumCD↑, dose dependent manner
ER Stress↑,
GRP78/BiP↑,
p‑PERK↑, p-PERK
CHOP↑,
Ca+2↑, enhanced mitochondrial Ca2+ uptake
XBP-1↑,
p‑IRE1↑,

4759-

antiOx,

Chemo,

Potential Contributions of Antioxidants to Cancer Therapy: Immunomodulation and Radiosensitization

Review,

Var,

TumCD↑, curcumin has been shown to modulate immunoediting processes including resurrecting immune surveillance mechanisms to help eradicate cancer cells
TumCG↓, studies by Lee-Chang et al34 have shown that administration of resveratrol, a dietary polyphenol compound possessing antioxidant properties at low doses that are nontoxic to immune cells, inhibits lung metastasis of breast cancer tumor.
ROS⇅, Of importance, resveratrol can exert both antioxidant and pro-oxidant properties depending on its concentration and cell types used
eff↑, Wang et al36 have demonstrated that a combination of fish oil and selenium that possesses anti-inflammatory and antioxidant activities exerted synergistic effects in suppressing lung tumor growth mediated via decreasing the population of splenic Treg
RadioS↑, Several nutritional cancer chemopreventive compounds having antioxidant properties have been documented to potentiate radiation therapy–induced cytotoxic effects on cancer cells while reducing its toxicity on normal surrounding tissues.77-86
TumCG↓, soy isoflavone component genistein on prostate cancer demonstrated that both soy and genistein inhibited the growth of in vitro human PC-3 prostate cancer cells and in vivo orthotopic PC-3 tumors
OS↑, While a statistically significant improved survival rate either at 1 year or 5 years was associated with melatonin supplementation
toxicity∅, 9 RCTs reported no differences in the toxicities by antioxidants supplementation
toxicity↑, and 1 RCT with vitamin A reported increased toxicity.

2635-

Api,

CUR,

Synergistic Effect of Apigenin and Curcumin on Apoptosis, Paraptosis and Autophagy-related Cell Death in HeLa Cells

in-vitro,

Cerv,

HeLa

TumCD↑, Treatment with a combination of apigenin and curcumin increased the expression levels of genes related to cell death in HeLa cells 1.29- to 27.6-fold.
eff↑, combination of curcumin and apigenin showed a synergistic anti-tumor effect
TumAuto↑, autophagic cell death, as well as ER stress-associated paraptosis
ER Stress↑,
Paraptosis↑,
GRP78/BiP↓, GRP78 expression was down-regulated, and massive cytoplasmic vacuolization was observed in HeLa cells
Dose↝, combined use of 0.09 μg/μl curcumin and 0.06 μg/μl apigenin showed a synergistic anti-tumor effect

2638-

Api,

Apigenin, by activating p53 and inhibiting STAT3, modulates the balance between pro-apoptotic and pro-survival pathways to induce PEL cell death

in-vitro,

lymphoma,

PEL

TumCD↑, We show that apigenin induced PEL cell death and autophagy along with reduction of intracellular ROS.
TumAuto↑,
ROS↓,
P53↑, Mechanistically, apigenin activated p53 that induced catalase, a ROS scavenger enzyme, and inhibited STAT3, the most important pro-survival pathway in PEL, as assessed by p53 silencing.
Catalase↑,
STAT3↓,

3160-

Ash,

Withaferin A: A Pleiotropic Anticancer Agent from the Indian Medicinal Plant Withania somnifera (L.) Dunal

Review,

Var,

TumCCA↑, withaferin A suppressed cell proliferation in prostate, ovarian, breast, gastric, leukemic, and melanoma cancer cells and osteosarcomas by stimulating the inhibition of the cell cycle at several stages, including G0/G1 [86], G2, and M phase
H3↑, via the upregulation of phosphorylated Aurora B, H3, p21, and Wee-1, and the downregulation of A2, B1, and E2 cyclins, Cdc2 (Tyr15), phosphorylated Chk1, and Chk2 in DU-145 and PC-3 prostate cancer cells.
P21↑,
cycA1/CCNA1↓,
CycB/CCNB1↓,
cycE/CCNE↓,
CDC2↓,
CHK1↓,
Chk2↓,
p38↑, nitiated cell death in the leukemia cells by increasing the expression of p38 mitogen-activated protein kinases (MAPK)
MAPK↑,
E6↓, educed the expression of human papillomavirus E6/E7 oncogenes in cervical cancer cells
E7↓,
P53↑, restored the p53 pathway causing the apoptosis of cervical cancer cells.
Akt↓, oral dose of 3–5 mg/kg withaferin A attenuated the activation of Akt and stimulated Forkhead Box-O3a (FOXO3a)-mediated prostate apoptotic response-4 (Par-4) activation,
FOXO3↑,
ROS↑, the generation of reactive oxygen species, histone H2AX phosphorylation, and mitochondrial membrane depolarization, indicating that withaferin A can cause the oxidative stress-mediated killing of oral cancer cells [
γH2AX↑,
MMP↓,
mitResp↓, withaferin A inhibited the expansion of MCF-7 and MDA-MB-231 human breast cancer cells by ROS production, owing to mitochondrial respiration inhibition
eff↑, combination treatment of withaferin A and hyperthermia induced the death of HeLa cells via a decrease in the mitochondrial transmembrane potential and the downregulation of the antiapoptotic protein myeloid-cell leukemia 1 (MCL-1)
TumCD↑,
Mcl-1↓,
ER Stress↑, . Withaferin A also attenuated the development of glioblastoma multiforme (GBM), both in vitro and in vivo, by inducing endoplasmic reticulum stress via activating the transcription factor 4-ATF3-C/EBP homologous protein (ATF4-ATF3-CHOP)
ATF4↑,
ATF3↑,
CHOP↑,
NOTCH↓, modulating the Notch-1 signaling pathway and the downregulation of Akt/NF-κB/Bcl-2 . withaferin A inhibited the Notch signaling pathway
NF-kB↓,
Bcl-2↓,
STAT3↓, Withaferin A also constitutively inhibited interleukin-6-induced phosphorylation of STAT3,
CDK1↓, lowering the levels of cyclin-dependent Cdk1, Cdc25C, and Cdc25B proteins,
β-catenin/ZEB1↓, downregulation of p-Akt expression, β-catenin, N-cadherin and epithelial to the mesenchymal transition (EMT) markers
N-cadherin↓,
EMT↓,
Cyt‑c↑, depolarization and production of ROS, which led to the release of cytochrome c into the cytosol,
eff↑, combinatorial effect of withaferin A and sulforaphane was also observed in MDA-MB-231 and MCF-7 breast cancer cells, with a dramatic reduction of the expression of the antiapoptotic protein Bcl-2 and an increase in the pro-apoptotic Bax level, thus p
CDK4↓, downregulates the levels of cyclin D1, CDK4, and pRB, and upregulates the levels of E2F mRNA and tumor suppressor p21, independently of p53
p‑RB1↓,
PARP↑, upregulation of Bax and cytochrome c, downregulation of Bcl-2, and activation of PARP, caspase-3, and caspase-9 cleavage
cl‑Casp3↑,
cl‑Casp9↑,
NRF2↑, withaferin A binding with Keap1 causes an increase in the nuclear factor erythroid 2-related factor 2 (Nrf2) protein levels, which in turn, regulates the expression of antioxidant proteins that can protect the cells from oxidative stress.
ER-α36↓, Decreased ER-α
LDHA↓, inhibited growth, LDHA activity, and apoptotic induction
lipid-P↑, induction of oxidative stress, increased lipid peroxidation,
AP-1↓, anti-inflammatory qualities of withaferin A are specifically attributed to its inhibition of pro-inflammatory molecules, α-2 macroglobulin, NF-κB, activator protein 1 (AP-1), and cyclooxygenase-2 (COX-2) inhibition,
COX2↓,
RenoP↑, showing strong evidence of the renoprotective potential of withaferin A due to its anti-inflammatory activity
PDGFR-BB↓, attenuating the BB-(PDGF-BB) platelet growth factor
SIRT3↑, by increasing the sirtuin3 (SIRT3) expression
MMP2↓, withaferin A inhibits matrix metalloproteinase-2 (MMP-2) and MMP-9,
MMP9↓,
NADPH↑, but also provokes mRNA stimulation for a set of antioxidant genes, such as NADPH quinone dehydrogenase 1 (NQO1), glutathione-disulfide reductase (GSR), Nrf2, heme oxygenase 1 (HMOX1),
NQO1↑,
GSR↑,
HO-1↑,
*SOD2↑, cardiac ischemia-reperfusion injury model. Withaferin A triggered the upregulation of superoxide dismutase SOD2, SOD3, and peroxiredoxin 1(Prdx-1).
*Prx↑,
*Casp3?, and ameliorated cardiomyocyte caspase-3 activity
eff↑, combination with doxorubicin (DOX), is also responsible for the excessive generation of ROS
Snail↓, inhibition of EMT markers, such as Snail, Slug, β-catenin, and vimentin.
Slug↓,
Vim↓,
CSCs↓, highly effective in eliminating cancer stem cells (CSC) that expressed cell surface markers, such as CD24, CD34, CD44, CD117, and Oct4 while downregulating Notch1, Hes1, and Hey1 genes;
HEY1↓,
MMPs↓, downregulate the expression of MMPs and VEGF, as well as reduce vimentin, N-cadherin cytoskeleton proteins,
VEGF↓,
uPA↓, and protease u-PA involved in the cancer cell metastasis
*toxicity↓, A was orally administered to Wistar rats at a dose of 2000 mg/kg/day and had no adverse effects on the animals
CDK2↓, downregulated the activation of Bcl-2, CDK2, and cyclin D1
CDK4↓, Another study also demonstrated the inhibition of Hsp90 by withaferin A in a pancreatic cancer cell line through the degradation of Akt, cyclin-dependent kinase 4 Cdk4,
HSP90↓,

2003-

Ash,

Withaferin A Induces Cell Death Selectively in Androgen-Independent Prostate Cancer Cells but Not in Normal Fibroblast Cells

in-vitro,

Pca,

PC3

2 μM WA

in-vitro,

Pca,

DU145

in-vitro,

Nor,

TIG-1

in-vitro,

PC,

LNCaP

TumCD↑, We report here that 2 μM WA induced cell death selectively in androgen-insensitive PC-3 and DU-145 prostate adenocarcinoma cells
selectivity↑, whereas its toxicity was less severe in androgen-sensitive LNCaP prostate adenocarcinoma cells and normal human fibroblasts (TIG-1 and KD)
cFos↑, WA significantly increased mRNA levels of c-Fos and 11 heat-shock proteins (HSPs) in PC-3 and DU-145, but not in LNCaP and TIG-1.
ROS↑, WA induced generation of reactive oxygen species (ROS) in PC-3 and DU-145, but not in normal fibroblasts
*ROS∅, but not in normal fibroblasts
HSP70/HSPA5↑,
Apoptosis↑, WA induces apoptosis mediated by ER stress
ER Stress↑,
TumCCA↑, WA induces autophagy in breast cancer cells, but the detailed mechanism remains elusive

4819-

ASTX,

Astaxanthin Induces Apoptosis in MCF-7 Cells through a p53-Dependent Pathway

in-vitro,

BC,

MCF-7

5, 10, 25, 50, 75, 100, 125, and 150 μg/mL)

IC50 = 89.742 μg/mL

antiOx↑, It is well known that AXT plays a role as a drug with antioxidant and antitumor properties
AntiTum↑,
TumCD↑, The treatment induced the decrease in cell number in a dose-dependent manner
P53↑, it was observed that the expression of p53 and p21 increased proportionally to the concentration of the AXT treatment.
P21↑,
Apoptosis↑, These findings suggest that the apoptosis of MCF-7 cells induced by AXT operates through a p53-dependent pathway, implying that AXT could potentially have a beneficial role in future breast cancer treatments.
Dose↝, Treatment with 50 μg/mL of AXT led to a viability of the tumor cell of approximately 30% after 48 h.
Casp3↑, The results indicated that caspase-3 activity increased following AXT treatment, reaching a maximum at 48 h post treatment

4818-

ASTX,

MEL,

Effect of astaxanthin and melatonin on cell viability and DNA damage in human breast cancer cell lines

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

T47D

in-vitro,

Nor,

MCF10

TumCD↑, Astaxanthin increases the melatonin-induced cell death in breast cancer cells
DNAdam↑, Astaxanthin-melatonin combination and DNA damages in breast cancer cells
*antiOx↑, strong anti-oxidative, anti-tumoral, and anti-inflammatory effects.
*AntiTum↑,
Inflam↓,
tumCV↓, Astaxanthin at lower doses than melatonin reduced cell viability and Bcl2 expression, induced apoptosis and DNA damage in MDA-MB-231 and T47D.
Bcl-2↓,
Apoptosis↓,
selectivity↑, Meanwhile, the effects of astaxanthin on cell cytotoxicity, apoptosis, and DNA damage in MCF10A cells are insignificant compared to MDA-MB-231 and T47D.
eff↑, Furthermore, the presence of astaxanthin increased the function of melatonin-induced cell death in breast cancer cells.
Dose↓, The results showed that very low doses of astaxanthin reduced survival rate, induced apoptosis, reduced the expression of Bcl2 proteins, and destroyed the DNA in cancerous cells

4807-

ASTX,

An overview of the anticancer activity of astaxanthin and the associated cellular and molecular mechanisms

Review,

Var,

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

5362-

AV,

Anti-cancer effects of aloe-emodin: a systematic review

Review,

Var,

AntiCan↑, Aloe-emodin possesses multiple anti-proliferative and anti-carcinogenic properties in a host of human cancer cell lines, with often multiple vital pathways affected by the same molecule.
eff↝, The effects of aloe-emodin are not ubiquitous across all cell lines but depend on cell type.
TumCP↓, most notable effects include inhibition of cell proliferation, migration, and invasion; cycle arrest; induction of cell death;
TumCMig↓,
TumCI↓,
TumCCA↑,
TumCD↑,
MMP↓, mitochondrial membrane and redox perturbations; and modulation of immune signaling.
ROS↑, which coincide with deleterious effects on mitochondrial membrane permea-bility and/or oxidative stress via exacerbated ROS production.
Apoptosis↑, In bladder cancer cells (T24), aloe-emodin induced time-and dose-dependent apoptosis [7]
CDK1↓, reduced levels of cyclin-dependent kinase (CDK) 1, cyclin B1, and BCL-2 after treatment with aloe-emodin.
CycB/CCNB1↓,
Bcl-2↓,
PCNA↓, Increases in cyclin B1, CDK1, and alkaline phosphatase (ALP) activity were observed along with inhibition of proliferating cell nuclear antigen (PCNA), showing decreased proliferation.
ATP↓, human lung non-small cell car¬cinoma (H460). They found a time- de¬pendent reduction in ATP, lower ATP synthase expression
ER Stress↑, hypothesized to cause apoptosis by augmenting endoplasmic reticulum stress [16].
cl‑Casp3↑, (HepG2) cells underwent apoptosis through a cas-pase-dependent pathway with cleavage and activation of caspases-3/9 and cleavage of PARP [24]
cl‑Casp9↑,
cl‑PARP↑,
MMP2↓, Matrix metalloproteinase-2 was significantly decreased, with an increase in ROS and cytosolic calcium.
Ca+2↑,
DNAdam↑, U87 malignant glioma cells through disruption of mitochondrial membrane potential, cell cycle arrest in the S phase, and DNA fragmentation in a time-dependent manner with minimal necrosis
Akt↓, Prostate cancer. Following treatment with aloe-emodin, mTORC2's down¬stream enzymes, AKT and PKCa, were inhibited
PKCδ↓,
mTORC2↓, Proliferation of PC3 cells was inhibited as a result of aloe-emodin binding to mTORC2, with inhibition of mTORC2 kinase activity.
GSH↓, Skin cancer. Intracellular ROS increased, while intra-cellular-reduced glutathione (GSH) was depleted and BCL-2 (anti-apoptotic protein) was down-regulated.
ChemoSen↑, Aloe-emodin also sensitizes skin cancer cells to chemo-therapy. aloe-emodin and emodin potentiated the therapeutic effects of cisplatin, doxo-rubicin, 5-fluorouracil

1523-

Ba,

Baicalein induces human osteosarcoma cell line MG-63 apoptosis via ROS-induced BNIP3 expression

in-vitro,

OS,

MG63

(12.5, 25, and 50 μM)

in-vitro,

Nor,

hFOB1.19

TumCD↑,
Apoptosis↑,
ROS↑, baicalein activated apoptosis through induced intracellular reactive oxygen species (ROS) generation
eff↓, and that ROS scavenger N-acetyl-cysteine (NAC), glutathione (GSH), and superoxide dismutase (SOD) apparently inhibited intracellular ROS production, consequently attenuating the baicalein-induced apoptosis.
Casp3↑, Baicalein treatment markedly increased active caspase-3 expression
Bcl-2↓,
selectivity↑, baicalein influenced little growth reduction of hFOB1.19 cells. (normal cells)
Cyt‑c↑, release of cytochrome c from mitochondrial to cytosol
LDH?, (25 and 50 μM) induced increases of LDH release (2.2- and 3.6-folds) which showed the cytotoxicity of baicalein
BNIP3?, we conclude that baicalein induces ROS production and BNIP3 expression with the subsequent activation of Bax
BAX↑,

2023-

BBR,

Berberine Induces Caspase-Independent Cell Death in Colon Tumor Cells through Activation of Apoptosis-Inducing Factor

in-vitro,

Colon,

0-100uM

in-vitro,

Nor,

YAMC

TumCD↑, Berberine decreased colon tumor colony formation in agar, and induced cell death and LDH release in a time- and concentration-dependent manner in IMCE cells.
*toxicity↓, In contrast, YAMC(normal) cells were not sensitive to berberine-induced cell death. less cytotoxic effects on normal colon epithelial cells.
selectivity↑, see figure 2
ROS↑, berberine-stimulated ROS production
*ROS∅, ROS production in a concentration-dependent manner only in IMCE cells, but not in YAMC cells. In YAMC cells, berberine did not induce ROS production
MMP↓, berberine induced mitochondrial depolarization in a concentration-dependent manner in IMCE cells, but not in YAMC cells
*MMP∅, but not in YAMC cells
PARP↑, Berberine Activation of PARP
BioAv↝, absorption of berberine by YAMC is lower than that by IMCE cells

2680-

BBR,

PDT,

Photodynamic therapy-triggered nuclear translocation of berberine from mitochondria leads to liver cancer cell death

in-vitro,

Liver,

HUH7

TumCD↑, blue light irradiation (488 nm). The results showed that berberine rapidly translocated from the mitochondria to the nucleus upon light exposure, ultimately inducing cell death in SNU449 and Huh7 cells.
ROS↑, Additionally, we observed a significant increase in reactive oxygen species, linking the phototoxic effects to oxidative stress
TumCCA↑, indicating cell cycle arrest following treatment with berberine and PDT
ER Stress↑, Western blotting confirmed that ER stress was significantly induced

2719-

BetA,

Betulinic Acid Restricts Human Bladder Cancer Cell Proliferation In Vitro by Inducing Caspase-Dependent Cell Death and Cell Cycle Arrest, and Decreasing Metastatic Potential

in-vitro,

CRC,

T24/HTB-9

30 μg/mL BA for 48 h

in-vitro,

Bladder,

UMUC3

33.2 μg/mL

in-vitro,

Bladder,

5637

 28.5 μg/mL

TumCD↑, BA induced cell death in bladder cancer cells and that are accompanied by apoptosis, necrosis, and cell cycle arrest.
Apoptosis↑,
TumCCA↑,
CycB/CCNB1↓, BA decreased the expression of cell cycle regulators, such as cyclin B1, cyclin A, cyclin-dependent kinase (Cdk) 2, cell division cycle (Cdc) 2, and Cdc25c
cycA1/CCNA1↓,
CDK2↓,
CDC25↓,
mtDam↑, BA-induced apoptosis was associated with mitochondrial dysfunction that is caused by loss of mitochondrial membrane potential, which led to the activation of mitochondrial-mediated intrinsic pathway.
BAX↑, BA up-regulated the expression of Bcl-2-accociated X protein (Bax) and cleaved poly-ADP ribose polymerase (PARP), and subsequently activated caspase-3, -8, and -9.
cl‑PARP↑,
Casp3↑,
Casp8↑,
Casp9↑,
Snail↓, decreased the expression of Snail and Slug in T24 and 5637 cells, and matrix metalloproteinase (MMP)-9 in UMUC-3 cells.
Slug↓,
MMP9↓,
selectivity↑, Among the bladder cancer cell lines, 5637 cells were much more sensitive to BA than T24 or UMUC-3 cells under the same conditions. However, BA does not affect cell growth in normal cell lines including RAW 264.7
MMP↓, BA Induces Loss of Mitochondrial Membrane Potential (MMP, ΔΨm) in Human Bladder Cancer Cells
ROS∅, As a result, we found that BA did not affect intracellular ROS levels in all three bladder cancer cells. In addition, BA-induced cell viability inhibition was not restored by NAC pre-treatment
TumCMig↓, BA Decreases Migration and Invasion of Human Bladder Cancer Cells
TumCI↓,

2716-

BetA,

Cellular and molecular mechanisms underlying the potential of betulinic acid in cancer prevention and treatment

Review,

Var,

AntiCan↑, BA has a range of well-documented pharmacological and biological effects, including antibacterial, immunomodulatory, diuretic, antiviral, antiparasitic, antidiabetic, and anticancer activities
TumCD↑, anticancer properties of BA are mediated by the activation of cell death and cell cycle arrest, production of reactive oxygen species, increased mitochondrial permeability, modulation of nuclear factor-κB and Bcl-2 family signaling
TumCCA↑,
ROS↑,
NF-kB↓,
Bcl-2↓,
Half-Life↝, The half-life eliminations were 11.8 and 11.5 h after 500 and 250 mg/kg of intraperitoneal (i.p.) BA administration
GLUT1↓, the expression of HIF target genes, such as GLUT1, VEGF, and PDK1 was also suppressed by BA
VEGF↓,
PDK1↓,

5715-

BF,

Bufalin for an innovative therapeutic approach against cancer

Review,

Var,

selectivity↑, All leads to the conclusion that bufalin mediates its effects by affecting all the hallmarks of cancer and seems restricted to cancer cells avoiding side effects.
TumCP↓, Bufalin decreases cancer cell proliferation by acting on the cell cycle and inducing different mechanisms of cell death including apoptosis, necroptosis, autophagy and senescence.
TumCCA↓,
TumCD↑,
Apoptosis↑,
TumAuto↑,
TumMeta↓, Bufalin also moderates metastasis formation by blocking migration and invasion as well as angiogenesis and by inducing a phenotype switch towards differentiation and decreasing cancer cell stemness.
TumCMig↓,
TumCI↓,
angioG↓,
CSCs↓,

5476-

BM,

In Vitro Synergistic Inhibition of HT-29 Proliferation and 2H-11 and HUVEC Tubulogenesis by Bacopaside I and II Is Associated with Ca2+ Flux and Loss of Plasma Membrane Integrity

vitro+vivo,

CRC,

HT29

TumCD↑, triterpene saponin bacopaside (bac) II, purified from the medicinal herb Bacopa monnieri, induced cell death in colorectal cancer cell lines and reduced endothelial cell migration and tube formation,
TumCMig↓,
Ca+2↑, although an increase in cytosolic Ca2+ was detected in all three cell lines.

745-

Bor,

Investigation of cytotoxic antiproliferative and antiapoptotic effects of nanosized boron phosphate filled sodium alginate composite on glioblastoma cancer cells

in-vitro,

GBM,

U87MG

in-vitro,

Nor,

L929

in-vitro,

GBM,

T98G

TumCD↑,
*toxicity↓, did not affect healthy fibroblast cells but had a cytotoxic effect on glioblastoma cells

1640-

CA,

MET,

Caffeic Acid Targets AMPK Signaling and Regulates Tricarboxylic Acid Cycle Anaplerosis while Metformin Downregulates HIF-1α-Induced Glycolytic Enzymes in Human Cervical Squamous Cell Carcinoma Lines

in-vitro,

Cerv,

SiHa

GLS↓, downregulation of Glutaminase (GLS) and Malic Enzyme 1 (ME1)
NADPH↓, CA alone and co-treated with Met caused significant reduction of NADPH
ROS↑, increased ROS formation and enhanced cell death
TumCD↑,
AMPK↑, activation of AMPK
Hif1a↓, Met inhibited Hypoxia-inducible Factor 1 (HIF-1α). CA treatment at 100 μM for 24 h also inhibited HIF-1α
GLUT1↓,
GLUT3↓,
HK2↓,
PFK↓, PFKFB4
PKM2↓,
LDH↓,
cMyc↓, Met suppressed the expression of c-Myc, BAX and cyclin-D1 (CCND1) a
BAX↓,
cycD1/CCND1↓,
PDH↓, CA at a concentration of 100 µM caused inhibition of PDK activity
ROS↑, CA Regulates TCA Cycle Supply via Pyruvate Dehydrogenase Complex (PDH), Induces Mitochondrial ROS Generation and Evokes Apoptosis
Apoptosis↑,
eff↑, both drugs inhibited the expression of ACLY and FAS, but the greatest effect was detected after co-treatment
ACLY↓,
FASN↓,
Bcl-2↓,
Glycolysis↓, Met acts as a glycolytic inhibitor under normoxic and hypoxic conditions

5746-

CA,

Caffeic acid hinders the proliferation and migration through inhibition of IL-6 mediated JAK-STAT-3 signaling axis in human prostate cancer

in-vitro,

Pca,

PC3

in-vitro,

Pca,

LNCaP

tumCV↓, CA inhibits prostate cancer cells (PC-3 and LNCaP) proliferation and induces reactive oxygen species (ROS), cell cycle arrest, and apoptosis cell death in a concentration-dependent manner.
ROS↑,
TumCCA↑, CA induces ROS production, G2/M cell cycle arrest and apoptotic cell death in prostate cancer cells
Apoptosis↑,
p‑MAPK↓, CA treatment alleviates the expression phosphorylated form of MAPK families, i.e., extracellular signal-regulated kinase 1 (ERK1), c-Jun N-terminal kinase (JNK), and p38 in PC-3 cells.
ERK↓,
JNK↓,
p38↓,
IL6↓, CA inhibits the expression of IL-6, JAK1, and phosphorylated STAT-3 in both PC-3 and LNCaP cells.
JAK1↓,
p‑STAT3↓,
cycD1/CCND1↓, it resulted in decreased expression of cyclin-D1, cyclin-D2, and CDK1 in both PC-3 cells.
CDK1↓,
BAX↑, CA induces apoptosis by enhancing the expression of Bax and caspase-3; and decreased expression of Bcl-2 in prostate cancer cells.
Casp3↑,
Bcl-2↓,
TumCD↑, CA induces cell death and inhibits colony formation in prostate cancer cells

5923-

CA,

RosA,

Rosemary as a Potential Source of Natural Antioxidants and Anticancer Agents: A Molecular Docking Study

Review,

Var,

TumCD↑, CA, it has the capacity to induce cell death of cancer cells through the rise in ROS levels within the cells, the inhibition of protein kinase AKT, the activation of autophagy-related genes (ATG) and the disrupt mitochondrial membrane potential.
ROS↑,
Akt↓,
ATG3↑,
MMP↓,
Casp↑, RA, its antitumor actions encompass apoptosis induction through caspase activation, the inhibition of cell proliferation by interrupting cell cycle progression and epigenetic regulation, antioxidative stress-induced DNA damage, and interference with
TumCP↓,
TumCCA↑,
DNAdam↑,
angioG↓,

5849-

CAP,

The Impact of TRPV1 on Cancer Pathogenesis and Therapy: A Systematic Review

Review,

Var,

TRPV1↑, TRPV1 belongs to the transient receptor potential channel vanilloid subfamily and is also known as the capsaicin receptor and vanilloid receptor 1 (VR1).
Ca+2↑, The activation of TRPV1 induces the cellular influx of Ca2+ and Na+ ions 17-19, and the excess intracellular Ca2+ and Na+ leads to cell death 20.
TumCD↑,
TumCCA↑, Induced cell cycle arrest in G0/G1 phase and apoptosis by activating p53 to upregulate Fas/CD95 in TRPV1-overexpressing cells
Apoptosis↑,
P53↑,
Fas↑,
PI3K↑, Activated PI3K and p44/42 MAPK pathways to suppress ceramide production and increased androgen receptor expression
AR↑,
STAT3↓, attenuating STAT3 phosphorylation
ROS↑, Induced apoptosis by producing ROS originating from the mitochondria
MMP↓, Disrupted mitochondrial membrane potential and suppressed ATP synthesis to induce apoptosis
ATP↓,
CHOP↑, Stimulated ROS generation, increased CHOP expression level, and promoted apoptosis
TumCMig↓, As TRPV1 serves as the main Ca2+-influx channel, it is reasonable to suggest that TRPV1 could act as an enhancer or inhibitor of migration and invasion in a tissue- or cell-specific manner.
Twist↓, Capsaicin downregulated Tiwst1, Snail1, MMP2, and MMP9 and upregulated E-cadherin
Snail↓,
MMP2↓,
MMP9↓,
E-cadherin↑,

5944-

Cela,

HSP90 inhibitor, celastrol, arrests human monocytic leukemia cell U937 at G0/G1 in thiol-containing agents reversible way

in-vitro,

AML,

U937

TumCP↓, Celastrol affected the proliferation of U937 in a dose-dependent way, arresting the cell cycle at G0/G1 with 400 nM doses and triggering cell death with doses above 1000 nM.
TumCCA↑,
TumCD↑,
HSP90↓, Cell cycle arrest was accompanied by inhibition of HSP90 ATPase activity and elevation in HSP70 levels (a biochemical hallmark of HSP90 inhibition),
HSP70/HSPA5↑,
cycD1/CCND1↓, reduction in Cyclin D1, Cdk4 and Cdk6 levels
CDK4↓,
CDK6↓,
ATPase↓, celastrol's effects on ATPase activity in the protein complex pulled-down by anti-HSP90

5991-

Chit,

Chitosan-Based Nanoencapsulated Essential Oils: Potential Leads against Breast Cancer Cells in Preclinical Studies

Review,

BC,

*other↝, CS typically exhibits molecular weights ranging from 300 to 1000 kDa, influenced by its degree of acetylation.
*BioAv↓, Generally, CS is insoluble in water at neutral pH
eff↑, This pH-responsive solubility can be advantageous in drug delivery to specific regions of the body with varying pH levels
toxicity↓, It is non-toxic, biodegradable, and biocompatible.
eff↑, Owing to the favourable attributes of CS, it is widely used in the nanoencapsulation of EOs.
TumCD↑, CS nanoparticles have shown potent cytotoxic effects against human breast cancer MCF-7 cells with an IC50 ranging from 3.72 to 17.81 μg/mL after a 72 h incubation period.
Half-Life↑, It was reported that EO-loaded CS nanoparticles are able to circulate in the bloodstream for a relatively long time and accumulate at the cancer cell site
selectivity↑,
EPR↑, This can be achieved through the enhanced permeability and retention (EPR) effect.
ROS↑, Z. multiflora EO-loaded CS nanoparticles triggered the production of intracellular reactive oxygen species (ROS) in the mitochondria, which leads to apoptosis.
Apoptosis↑,
eff↑, CS-nanoencapsulated Citrus EOs exhibited improved cytotoxic properties against cancerous MDA-MB-468 cells.

6075-

CHL,

docx,

The effect of the combination therapy with chlorophyllin, a glutathione transferase P1-1 inhibitor, and docetaxel on triple-negative breast cancer invasion and metastasis in vivo/in vitro

vitro+vivo,

BC,

4T1

TumCMig↓, the coadministration of chlorophyllin and docetaxel significantly inhibited cell migration in vitro.
eff↑, coadministration of chlorophyllin and docetaxel may have a potential role in controlling metastatic processes by suppressing cell migration, gelatinase activity, and micrometastasis formation in triple-negative breast cancers.
TumMeta↓,
TumCCA↑, We found that while the docetaxel decreased the G0/G1 phase, both chlorophyllin and its coadministration with docetaxel led to a slight increase in the G0/G1 phase
Trx↓, In a study, it is shown that chlorophyllin inhibits the cellular thioredoxin reductase activity in a time-dependent manner in several cancer cell lines, induces ROS accumulation, and leads to cell death
ROS↓,
TumCD↑,
GSTP1/GSTπ↓, Chlorophyllin was shown to be a specific inhibitor of GSTP1.

2791-

CHr,

Chrysin attenuates progression of ovarian cancer cells by regulating signaling cascades and mitochondrial dysfunction

in-vitro,

Ovarian,

OV90

TumCP↓, chrysin inhibited ovarian cancer cell proliferation and induced cell death by increasing reactive oxygen species (ROS) production and cytoplasmic Ca2+ levels as well as inducing loss of mitochondrial membrane potential (MMP).
TumCD↑,
ROS↑,
Ca+2↑,
MMP↓,
MAPK↑, chrysin activated mitogen-activated protein kinase (MAPK) and phosphoinositide 3-kinase (PI3K)/AKT pathways in ES2 and OV90 cells in concentration-response experiments
PI3K↑, results indicate that the chrysin-induced activation of PI3K and MAPK signaling molecules, which induced apoptosis,
p‑Akt↑, Chrysin stimulated the phosphorylation of AKT and P70S6K proteins in both ES2 and OV90 cells compared to the untreated control cell
PCNA↓, treatment with chrysin attenuated the abundant expression of PCNA protein in both ES2 and OV90 cells
p‑p70S6↑,
p‑ERK↑, chrysin activated the phospho-ERK1/2, p38, and JNK proteins as members of the MAPK pathway in the ovarian cancer cells
p38↑,
JNK↑,
DNAdam↑, stimulates apoptotic events in prostate cancer cells by the accumulation of DNA fragmentation, an increase in the population of cells in the sub-G1 phase of the cell cycle
TumCCA↑,
chemoP↑, combination therapy with chrysin enhances the therapeutic effect of the chemotherapeutic agent, docetaxel, in lung cancer by reducing its adverse effects

4761-

CoQ10,

Elevated levels of mitochondrial CoQ10 induce ROS-mediated apoptosis in pancreatic cancer

in-vitro,

PC,

in-vivo,

PC,

MIA PaCa-2 xenograft mouse model

*ETC↝, Coenzyme Q10 is a critical cofactor in the electron transport chain with complex biological functions that extend beyond mitochondrial respiration.
ROS↑, This study demonstrates that delivery of oxidized Coenzyme Q10 (ubidecarenone) to increase mitochondrial Q-pool is associated with an increase in ROS generation, effectuating anti-cancer effects in a pancreatic cancer model.
*antiOx↑, In addition to its role in ETC function, CoQ10 has phenolic antioxidant activity via its ability to undergo hydrogen abstraction by free radicals6
ROS↑, Paradoxically, CoQ10 also exhibits pro-oxidant activity that occurs either due to a CoQ10 semiquinone reaction5 or due to a reaction with oxygen when CoQ10 is in its oxidized state
OCR↓, Delivery of supraphysiologic levels of ubidecarenone via BPM31510 decreases oxygen consumption rates (OCR) in pancreatic cancer
MMP↓, Ubidecarenone enhances succinate-dependent and glycerol-3-phosphate-dependent ROS generation, mitochondrial membrane depolarization, and regulated cell death
TumCD↑,
TumCG↓, BPM31510 (25 mg/kg, b.i.d) resulted in a significant decrease in tumour growth by day 45 after inoculation compared to saline-treated mice
other↝, NOTE: this is oxidized CoQ10, not the same as CoQ10!!!!!!

Showing Research Papers: 1 to 50 of 124
Page 1 of 3 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 124

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 186

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 4, Prx↑, 1, ROS∅, 2, SOD2↑, 1,

Mitochondria & Bioenergetics ⓘ

ETC↝, 1, MMP∅, 1,

Cell Death ⓘ

Casp3?, 1,

Transcription & Epigenetics ⓘ

other↝, 1,

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,

Functional Outcomes ⓘ

AntiTum↑, 1, neuroP↑, 1, toxicity↓, 3, toxicity↝, 2,

Infection & Microbiome ⓘ

Bacteria↓, 1,
Total Targets: 15

Scientific Paper Hit Count for: TumCD, Tumor Cell Death

21 Silver-NanoParticles
11 Magnetic Fields
9 Vitamin C (Ascorbic Acid)
8 Magnetic Field Rotating
6 Electrical Pulses
6 Selenite (Sodium)
5 Copper and Cu NanoParticles
4 Chemotherapy
4 Disulfiram
4 Phenethyl isothiocyanate
4 Quercetin
3 Astaxanthin
3 Melatonin
3 salinomycin
3 VitK3,menadione
2 3-bromopyruvate
2 Apigenin (mainly Parsley)
2 Curcumin
2 Ashwagandha(Withaferin A)
2 Berberine
2 Betulinic acid
2 Caffeic acid
2 Coenzyme Q10
2 diet FMD Fasting Mimicking Diet
2 Phenylbutyrate
1 2-DeoxyGlucose
1 Auranofin
1 Gold NanoParticles
1 Hyperthermia
1 Radiotherapy/Radiation
1 Anti-oxidants
1 Aloe anthraquinones
1 Baicalein
1 Photodynamic Therapy
1 Bufalin/Huachansu
1 Bacopa monnieri
1 Boron
1 Metformin
1 Carnosic acid
1 Rosmarinic acid
1 Capsaicin
1 Celastrol
1 chitosan
1 Chlorophyllin
1 Docetaxel
1 Chrysin
1 chemodynamic therapy
1 Date Fruit Extract
1 Emodin
1 Fenbendazole
1 Fisetin
1 Hydrogen Gas
1 Honokiol
1 Laetrile B17 Amygdalin
1 Luteolin
1 Methylene blue
1 SonoDynamic Therapy UltraSound
1 methotrexate
1 Nimbolide
1 Propyl gallate
1 Piperlongumine
1 Resveratrol
1 Pterostilbene
1 Selenium NanoParticles
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
1 Spermidine
1 Selenium
1 Thymoquinone
1 Urolithin
1 Magnesium
1 Whole Body Vibration

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

TumCD 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 ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Immune & Inflammatory Signaling ⓘ

Drug Metabolism & Resistance ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

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