Casp7 Cancer Research Results

Casp7, Caspase-7: Click to Expand ⟱

Source:

Type:

Members of the caspase family of proteases play essential roles in the initiation and execution of apoptosis. These caspases are divided into two groups: the initiator caspases (caspase-2, −8, −9 and −10), which are the first to be activated in response to a signal, and the executioner caspases (caspase-3, −6, and −7) that carry out the demolition phase of apoptosis. Downregulation of caspase-3 is an effective apoptosis-evading mechanism frequently observed in cancer cells in association with acquired chemoresistance to apoptosis-inducing anticancer drugs. Indeed, re-expression of caspase-3 often restores sensitivity to apoptosis.
Caspase-7:
Role: Executioner caspase similar to caspase-3.
Cancers: Expression levels can vary; often studied in breast and prostate cancers.
Prognosis: Its prognostic value is less clear and may depend on the cancer type.

Scientific Papers found: Click to Expand⟱

5459-

AF,

Auranofin Induces Lethality Driven by Reactive Oxygen Species in High-Grade Serous Ovarian Cancer Cells

in-vitro,

Ovarian,

ROS↑, AF primarily functions as a pro-oxidant by inhibiting thioredoxin reductase (TrxR), an antioxidant enzyme overexpressed in ovarian cancer.
TrxR↓, The primary mechanism of action of auranofin is to act as a pro-oxidative agent, increasing the production of reactive oxygen species (ROS) as a consequence of inhibiting the thioredoxin reductase (TrxR) anti-oxidant system
MMP↓, triggers the depolarization of the mitochondrial membrane, and kills HGSOC cells by inducing apoptosis.
Apoptosis↑,
eff↓, Notably, AF-induced cell death was abrogated by the ROS-scavenger N-acetyl cysteine (NAC).
Casp3↑, lethality of AF was associated with the activation of caspases-3/7 and the generation of DNA damage
Casp7↑,
DNAdam↑,
eff↑, Finally, when AF and L-BSO were combined, we observed synergistic lethality against HGSOC cells, which was mediated by a further increase in ROS and a decrease in the levels of the antioxidant GSH.
GSH↓,
angioG↓, Additionally, auranofin has been shown to inhibit angiogenesis
ChemoSen↑, In this study, we identified the mechanisms of cytotoxicity induced by auranofin in HGSOC cells that have different clinical sensitivities to platinum.
cl‑PARP↑, the cleavage of poly-ADP ribose polymerase (PARP), and the polyubiquitination of proteins
eff↑, synergistic lethal interaction between auranofin and a second pro-oxidant agent, the glutathione (GSH) inhibitor, L-buthionine sulfoximine (L-BSO);

5145-

AgNPs,

Silver nanoparticles induce irremediable endoplasmic reticulum stress leading to unfolded protein response dependent apoptosis in breast cancer cells

in-vitro,

BC,

MCF7

in-vitro,

BC,

T47D

Bacteria↓, Nowadays, silver nanoparticles (AgNP) are widely used in the medical field mainly for their antibacterial properties
Apoptosis↑, AgNP of 2 (AgNP2) and 15 nm (AgNP15) induce apoptosis in human MCF-7 and T-47D breast cancer cells.
ER Stress↑, Treatment with AgNP2 and AgNP15 led to accumulation and aggregation of misfolded proteins causing an endoplasmic reticulum (ER) stress and activating the unfolded protein response (UPR).
UPR↑,
PERK↑, The three main ER sensors, PERK, IRE-1α and ATF-6, were rapidly activated in response to AgNP2 and AgNP15
IRE1↑,
ATF6↑,
ATF4↑, AgNP2 and AgNP15 induced upregulation of the transcription factors ATF-4 and GADD153/CHOP
CHOP/DDIT3↑,
Casp9↑, Moreover, the initiating caspase-9 and the effector caspase-7 were activated in response to these NPs.
Casp7↑,
Mcl-1↓, In contrast, a downregulation of Mcl-1 and xIAP protein expression as well as a processing of PARP were observed.
XIAP↓,
PARP↝,
selectivity↑, Of note, the non-cancerous MCF-10A cells were more resistant to both AgNP2 and AgNP15 when compared to MCF-7 and T-47D cell lines.

351-

AgNPs,

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

in-vitro,

BC,

MCF7

 5ug/mL

in-vitro,

BC,

T47D

Casp9↑,
Casp3↑,
Casp7↑,
Bcl-2↓,

377-

AgNPs,

Anticancer Action of Silver Nanoparticles in SKBR3 Breast Cancer Cells through Promotion of Oxidative Stress and Apoptosis

in-vitro,

BC,

SkBr3

ROS↑,
Apoptosis↑,
Bax:Bcl2↑,
VEGF↑, VEGF-A
Akt↓,
PI3K↓,
TAC↓,
TOS↑,
OSI↑,
MDA↑,
Casp3↑,
Casp7↑,

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↑,

7399-

Amla,

Molecular Mechanisms of Cancer Prevention by Gooseberry (Phyllanthus emblica)

Review,

Var,

*Dose↝, P. emblica fruit is the second richest known source of vitamin C (4), as well as having high levels of tannins, alkaloids, polyphenols, vitamins, and minerals. P. emblica contains several biologically-active antioxidant polyphenols, including gallic
*Inflam↓, gooseberry constituents possess anti-inflammatory, anticancer, anti-microbial, and anti-oxidant effects which protect against neurological disorders, have hepatoprotective and cardioprotective activities, and are cancer-preventive
*AntiCan↑,
*antiOx↑,
*neuroP↑,
*hepatoP↑,
*cardioP↑,
*P450↓, via inhibition of cytochrome P450 (CYP450) isozymes
*SOD↑, figure 3
*GPx↑,
*Catalase↑,
*ROS↓,
*CD4+↑,
*CD19↑,
*NK cell↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
Fas↑,
BAX↑,
Bcl-2↓,
*IL10↑,
*TNF-α↓,
*IL6↓,
*iNOS↓,
*COX2/PTGS2↓,
*GSTs↑,
*NF-kB↓,
*AP-1↓,
*cJun↓,
*lipid-P↓, P. emblica extracts scavenge free radicals, protect against lipid peroxidation, and thus may play a role in preventing diseases associated with oxidative stress, including cancer.
TumCG↓, P. emblica extract (50–100 μg/ml) significantly inhibits the cell growth of human colorectal (SW620), lung (A549), breast (MDA-MB-231), cervical (HeLa), ovarian (SK-OV3), and liver (HepG2) cancer cell lines
DNAdam↑, apoptosis was induced by triggering of DNA fragmentation, caspase-3, −7, and −8 activity, and Fas protein expression
TumCCA↑, inducing G2/M phase cell cycle arrest and promoting apoptosis via increasing expression of Fas, FasL, and cleaved caspase-8
MMP2↓, P. emblica extract (1–3 µg/ml) decreases the expression of both MMP2 and MMP9 in human fibrosarcoma (HT1080) cells,
MMP9↓,

7407-

Amla,

Functional and Nutraceutical Significance of Amla (Phyllanthus emblica L.): A Review

Review,

Nor,

*Inflam↓, amla has been proven to have anti-hyperglycemic, hypoglycemic, anti-inflammatory, anti-hyperlipidemic, and antioxidant activities
*antiOx↑,
*GSH↑, a study using the extract from amla leaves (200–400 mg/kg BW) indicated a similar protective effect in diabetic mice by reducing inducing the activity of GSH, GPx, SOD, and CAT activity and also reducing lipid peroxidation
*GPx↑,
*SOD↑,
*Catalase↑,
*lipid-P↓, significant reduction in the peroxidation level and increased antioxidant status were observed in subjects that consumed 250 mg (twice a day) for 60 days
*ROS↓, polyphenols (especially tannins and flavonoids) present in this fruit extract significantly reduced oxidative stress by scavenging NOx.
*cardioP↑, Fruit Gallic acid Cardioprotective activity
*AntiDiabetic↑, Fruit Ellagic acid Antidiabetic activity
*neuroP↑, Fruit Emblicanin A and B Neuroprotective activity
*GastroP↑, Fruit Tannins and gallic acid Gastrointestinal protective activity
*COX2/PTGS2↓, inhibited the enhanced mitochondrial COX-2, MDA, and Bax expressions in the liver
*MDA↓,
*BAX↓,
*TG/TAG↓, Figure 2
*HDL↑,
*LDL↓,
*HMG-CoA↓,
*Dose↝, At the human level, a 500 mg dose of P. emblica L. extract (twice a day) for three months reduced the high sensitive C-reactive protein (CRP), total cholesterol, and LDL levels in Class I obese subjects
*CRP↓,
DNAdam↑, Particularly for amla extracts, DNA fragmentation, increased activity of caspase-3, 7, and 8, and up-regulation of Fas protein were observed in the HeLa cell line,
Casp3↑,
Casp7↑,
Casp8↑,
Fas↑,
TumCI↓, This study also indicated that P. emblica L. decreased the invasiveness of MDA-MB-231 cells (in vitro Matrigel invasion study), and no cytotoxicity was seen in normal lung fibroblasts (MRC5)
selectivity↑,

270-

Api,

Apigenin induces apoptosis in human leukemia cells and exhibits anti-leukemic activity in vivo via inactivation of Akt and activation of JNK

in-vivo,

AML,

U937

 20-40 uM (12/24h)

Akt↓, nactivation of Akt and activation of JNK
JNK↑,
Mcl-1↓,
cl‑Bcl-2↓, cleavage
Casp3↑,
Casp7↑,
Casp9↑,
cl‑PARP↑, cleaved
mTOR↓,
GSK‐3β↓,

2640-

Api,

Apigenin: A Promising Molecule for Cancer Prevention

Review,

Var,

chemoPv↑, considerable potential for apigenin to be developed as a cancer chemopreventive agent.
ITGB4↓, apigenin inhibits hepatocyte growth factor-induced MDA-MB-231 cells invasiveness and metastasis by blocking Akt, ERK, and JNK phosphorylation and also inhibits clustering of β-4-integrin function at actin rich adhesive site
TumCI↓,
TumMeta↓,
Akt↓,
ERK↓,
p‑JNK↓,
*Inflam↓, The anti-inflammatory properties of apigenin are evident in studies that have shown suppression of LPS-induced cyclooxygenase-2 and nitric oxide synthase-2 activity and expression in mouse macrophages
*PKCδ↓, Apigenin has been reported to inhibit protein kinase C activity, mitogen activated protein kinase (MAPK), transformation of C3HI mouse embryonic fibroblasts and the downstream oncogenes in v-Ha-ras-transformed NIH3T3 cells (43, 44).
*MAPK↓,
EGFR↓, Apigenin treatment has been shown to decrease the levels of phosphorylated EGFR tyrosine kinase and of other MAPK and their nuclear substrate c-myc, which causes apoptosis in anaplastic thyroid cancer cells
CK2↓, apigenin has been shown to inhibit the expression of casein kinase (CK)-2 in both human prostate and breast cancer cells
TumCCA↑, apigenin induces a reversible G2/M and G0/G1 arrest by inhibiting p34 (cdc2) kinase activity, accompanied by increased p53 protein stability
CDK1↓, inhibiting p34 (cdc2) kinase activity
P53↓,
P21↑, Apigenin has also been shown to induce WAF1/p21 levels resulting in cell cycle arrest and apoptosis in androgen-responsive human prostate cancer
Bax:Bcl2↑, Apigenin treatment has been shown to alter the Bax/Bcl-2 ratio in favor of apoptosis, associated with release of cytochrome c and induction of Apaf-1, which leads to caspase activation and PARP-cleavage
Cyt‑c↑,
APAF1↑,
Casp↑,
cl‑PARP↑,
VEGF↓, xposure of endothelial cells to apigenin results in suppression of the expression of VEGF, an important factor in angiogenesis via degradation of HIF-1α protein
Hif1a↓,
IGF-1↓, oral administration of apigenin suppresses the levels of IGF-I in prostate tumor xenografts and increases levels of IGFBP-3, a binding protein that sequesters IGF-I in vascular circulation
IGFBP3↑,
E-cadherin↑, apigenin exposure to human prostate carcinoma DU145 cells caused increase in protein levels of E-cadherin and inhibited nuclear translocation of β-catenin and its retention to the cytoplasm
β-catenin/ZEB1↓,
HSPs↓, targets of apigenin include heat shock proteins (61), telomerase (68), fatty acid synthase (69), matrix metalloproteinases (70), and aryl hydrocarbon receptor activity (71) HER2/neu (72), casein kinase 2 alpha
Telomerase↓,
FASN↓,
MMPs↓,
HER2/EBBR2↓,
CK2↓,
eff↑, The combination of sulforaphane and apigenin resulted in a synergistic induction of UGT1A1
AntiAg↑, Apigenin inhibit platelet function through several mechanisms including blockade of TxA
eff↑, ex vivo anti-platelet effect of aspirin in the presence of apigenin, which encourages the idea of the combined use of aspirin and apigenin in patients in which aspirin fails to properly suppress the TxA
FAK↓, Apigenin inhibits expression of focal adhesion kinase (FAK), migration and invasion of human ovarian cancer A2780 cells.
ROS↑, Apigenin generates reactive oxygen species, causes loss of mitochondrial Bcl-2 expression, increases mitochondrial permeability, causes cytochrome C release, and induces cleavage of caspase 3, 7, 8, and 9 and the concomitant cleavage of the inhibitor
Bcl-2↓,
Cyt‑c↑,
cl‑Casp3↑,
cl‑Casp7↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑IAP2/BIRC3↑,
AR↓, significant decrease in AR protein expression along with a decrease in intracellular and secreted forms of PSA. Apigenin treatment of LNCaP cells
PSA↓,
p‑pRB↓, apigenin inhibited hyperphosphorylation of the pRb protein
p‑GSK‐3β↓, Inhibition of p-Akt by apigenin resulted in decreased phosphorylation of GSK-3beta.
CDK4↓, both flavonoids exhibited cell growth inhibitory effects which were due to cell cycle arrest and downregulation of the expression of CDK4
ChemoSen↑, Combination therapy of gemcitabine and apigenin enhanced anti-tumor efficacy in pancreatic cancer cells (MiaPaca-2, AsPC-1)
Ca+2↑, apigenin in neuroblastoma SH-SY5Y cells resulted in increased apoptosis, which was associated with increases in intracellular free [Ca(2+)] and Bax:Bcl-2 ratio, mitochondrial release of cytochrome c and activation of caspase-9, calpain, caspase-3,12
cal2↑,

2474-

Ba,

Anticancer properties of baicalein: a review

Review,

Var,

in-vitro,

Nor,

BV2

ROS⇅, Like other flavonoids, baicalein can be either anti-oxidant or pro-oxidant, depending on its metabolism and concentration.
ROS↑, It is reported that baicalein generated ROS, subsequently caused endoplasmic reticulum (ER) stress, activated Ca2+-dependent mitochondrial death pathway, finally triggered apoptosis
ER Stress↑,
Ca+2↑,
Apoptosis↑,
eff↑, Due to this, ROS production is a mechanism shared by all non-surgical therapeutic approaches for cancer, including chemotherapy, radiotherapy and photodynamic therapy
DR5↑, baicalein-induced ROS generation up-regulated DR5 expression and then activated the extrinsic apoptotic pathway in human prostate cancer cells
12LOX↓, Baicalein is known as a 12-LOX inhibitor.
Cyt‑c↑, It markedly induced the release of Cytochrome c from mitochondria into the cytosol and activated Caspase-9, Caspase-7, and Caspase-3, concomitant with cleavage of the Caspase-3 substrate poly(ADP-ribose) polymerase
Casp7↑,
Casp9↑,
Casp3↑,
cl‑PARP↑,
TumCCA↑, Baicalein induces G1/S arrest due to increased Cyclin E expression, a major factor in the regulation of the G1/S checkpoint of the cell cycle, accompanied by reduced levels of Cdk 4 and Cyclin D1 in human lung squamous carcinoma (CH27) cells
cycE/CCNE↑,
CDK4↓,
cycD1/CCND1↓,
VEGF↓, In ovarian cancer cells, baicalein effectively lowered the protein level of VEGF, c-Myc, HIF-α, and NFκB
cMyc↓,
Hif1a↓,
NF-kB↓,
BioEnh↑, curcumin and high-dose (−)-epicatechin were demonstrated to subsequently increase the absorption of baicalein
BioEnh↑, Baicalein can increase the oral bioavailability of tamoxifen by inhibiting cytochrome P450 (CYP) 3A4-mediated metabolism of tamoxifen in the small intestine and/or liver,
P450↓,
*Hif1a↓, In BV2 microglia, baicalein suppressed expression of hypoxia-induced HIF-1α and hypoxia responsive genes, including inducible nitric oxide synthase (iNOS), COX-2, and VEGF, by inhibiting ROS and PI3K/Akt pathway (Hwang et al. 2008).
*iNOS↓,
*COX2/PTGS2↓,
*VEGF↓,
*ROS↓,
*PI3K↓,
*Akt↓,

2691-

BBR,

Berberine induces FasL-related apoptosis through p38 activation in KB human oral cancer cells

in-vitro,

Oral,

tumCV↓, viability of KB cells was found to decrease significantly in the presence of berberine in a dose-dependent manner.
DNAdam↑, berberine induced the fragmentation of genomic DNA, changes in cell morphology, and nuclear condensation.
Casp3↑, caspase-3 and -7 activation, and an increase in apoptosis were observed.
Casp7↑,
FasL↑, Berberine was also found to upregulate significantly the expression of the death receptor ligand, FasL
Casp8↑, triggered the activation of pro-apoptotic factors such as caspase-8, -9 and -3 and poly(ADP-ribose) polymerase (PARP).
Casp9↑,
PARP↑,
BAX↑, Bax, Bad and Apaf-1 were also significantly upregulated by berberine.
BAD↑,
APAF1↑,
MMP2↓, We also found that berberine-induced migration suppression was mediated by downregulation of MMP-2 and MMP-9 through phosphorylation of p38 MAPK.
MMP9↓,
p‑p38↑, This suggests that berberine-induced activation of the p38 and ERK1/2 MAPK pathways is the principal pathway involved in the apoptosis mediated by berberine in KB cells.
ERK↑,
MAPK↑,

5634-

BCA,

Molecular Mechanisms of Biochanin A in AML Cells: Apoptosis Induction and Pathway-Specific Regulation in U937 and THP-1

in-vitro,

AML,

U937

in-vitro,

AML,

THP1

Apoptosis↑, Biochanin A induced dose-dependent apoptosis, as evidenced by caspase-7 activation and PARP1 cleavage.
Casp7↑,
PARP1↑,
Bcl-2↓, Biochanin A downregulated oncogenes such as RUNX1, BCL2, and MYC while upregulating CHOP (GADD153), CDKN1A (p21), and SQSTM1 (p62), contributing to apoptosis and cell cycle arrest across both cell lines.
Myc↓,
CHOP/DDIT3↑,
P21↑,
p62↑,
TumCCA↑,
TXNIP↑, In contrast, in U937 cells, Biochanin A upregulated TXNIP and downregulated CCND2, highlighting the involvement of oxidative stress and G1/S cell cycle arrest.
ROS↑,
*antiOx↑, Biochanin A exhibits a broad spectrum of biological activities, including antioxidant, anti-inflammatory, estrogenic, metabolic regulatory, neuroprotective, and anticancer effects [1].
*Inflam↓,
*neuroP↑,
AntiCan↑,
TumCP↓, The anticancer mechanisms of Biochanin A involve the inhibition of cell proliferation via the modulation of cyclins and cyclin-dependent kinases
angioG↓, inhibition of angiogenesis and metastasis through downregulation of VEGF and matrix metalloproteinases (MMPs), and activation of apoptosis
TumMeta↓,
VEGF↓,
MMPs↓,
tumCV↓, Biochanin A significantly inhibited cell viability at concentrations ≥100 μM in U937 cells and ≥50 μM in THP-1 cells
DNAdam↑, Biochanin A induces a DNA damage response
CHOP/DDIT3↑, In our study, we observed a significant induction of CHOP protein expression following treatment with Biochanin A at concentrations of 100 μM and 200 μM.
cMyc↓, Biochanin A inhibited c-Myc protein expression in U937 and THP-1 cells
BioAv↓, Biochanin A remains limited due to its poor aqueous solubility and rapid systemic clearance, which render the 100–200 μM concentrations used in this study difficult to achieve in vivo
Half-Life↓,
BioAv↑, PEG-NLC formulations have been shown to significantly increase the plasma half-life and bioavailability of flavonoids

6509-

BCP,

βcaryophyllene oxide induces apoptosis and inhibits proliferation of A549 lung cancer cells

in-vitro,

Lung,

A549

tumCV↓, CPO was found to have an inhibitory concentration (IC50) of 124.1 ug/ml.
TumCP↓, Ki67 and PCNA were significantly inhibited after cells were treated with CPO at a concentration of 50 ug/ml compared to controls.
Ki-67↓,
PCNA↓,
P21↓, CPO-treated cells expressed more P21, P53, and DNA strand breaks than controls.
P53↑,
DNAdam↑,
TumCCA↑, accompanied by a significant cell cycle arrest in the S and G2/M phases.
Apoptosis↑, In treated A549 cells, this was also associated with a significant induction of apoptosis, as shown by the upregulation of the expression of caspases 3, 7, and 9, as well as Bax, and the downregulation of Bcl-2.
Casp3↑,
Casp7↑,
Casp9↑,
BAX↑,
Bcl-2↓,
GSH↑, redox status of treated A549 cells revealed a marked rise in GSH and GPx activity levels and a decline in 4-HNE levels, indicating low oxidative stress following CPO treatment of A549 cells.
GPx↑,
4-HNE↑,
ROS↓,
antiOx↑, CPO increased the antioxidants and decreased lipid peroxidation in A549 cells
lipid-P↓,

2755-

BetA,

Cytotoxic Potential of Betulinic Acid Fatty Esters and Their Liposomal Formulations: Targeting Breast, Colon, and Lung Cancer Cell Lines

in-vitro,

Colon,

HT29

in-vitro,

BC,

MCF7

in-vitro,

Lung,

H460

eff↑, BA-Lip exerted stronger cytotoxic effects than the parent compound,
Casp3↑, BA’s fatty esters and their respective liposomal formulations facilitated apoptosis in cancer cells by inducing nuclear morphological changes and increasing caspase-3/-7 activity.
Casp7↑,
NF-kB↓, BA antiproliferative effects against U87MG and A172 glioblastoma cells revealing the downregulation of the NF-κB pathway and upregulation of caspase-3 and -9, thus suggesting that apoptosis occurred through mitochondria-mediated mechanisms

2744-

BetA,

Betulin and betulinic acid: triterpenoids derivatives with a powerful biological potential

Review,

Var,

Apoptosis↓, Various studies have demonstrated that BE is able to induce apoptosis in numerous cancer cell lines (
TumCCA↑, 10 uM concentration, BE arrests cell cycle of murine melanoma B164A5 cells in S phase.
Casp9↑, BE is involved in the sequential activation of caspase-9, caspases 3 and 7, and cleaving of poly(ADP-ribose) polymerase (PARP) (Potze et al. 2014).
Casp3↑,
Casp7↑,
cl‑PARP↑,
MMP↓, mitochondrial membrane potential loss (Li et al. 2010; Potze et al. 2014).
ROS↑, increased reactive oxygen species (ROS) production
TOP1↓, BA was also shown to inhibit the proliferation of topoisomerases and therefore express anti-proliferative activity
NF-kB↓, BA was demonstrated to inhibit activating of NF-kB

5685-

BML,

The Therapeutic Effects of Bromelain against Colorectal Cancer: A Systematic Review

Review,

CRC,

TumCG↓, impeding tumor growth and metastasis
TumMeta↓,
ROS⇅, reducing mucins production/secretion and increasing/reducing reactive oxygen species (ROS) production.
Bcl-2↓, bromelain induces apoptosis via reduced expression of Bcl-2
Casp3↑, activation caspase system (caspase-3, 7, 8, and 9), and extranuclear p53.
Casp7↑,
Casp8↑,
Casp9↑,
P53↑,

5651-

BNL,

Cisplatin,

Natural borneol sensitizes human glioma cells to cisplatin-induced apoptosis by triggering ROS-mediated oxidative damage and regulation of MAPKs and PI3K/AKT pathway

in-vitro,

GBM,

U251

in-vitro,

GBM,

U87MG

ChemoSen↑, NB synergistically enhanced the anticancer efficacy of cisplatin in human glioma cells.
tumCV↓, Co-treatment of 40 μg/mL NB and 40 μg/mL cisplatin significantly inhibited U251 cell viability from 100% to 28.2% and increased the sub-G1 population from 1.4% to 59.3%.
TumCCA↑,
Apoptosis↑, NB enhanced cisplatin-induced apoptosis by activating caspases and triggering reactive oxygen species (ROS) overproduction
ROS↑,
DNAdam↑, ROS-mediated DNA damage was observed as reflected by the activation of ATM/ATR, p53 and histone.
ATR↑,
ATM↑,
P53↑,
Histones↑,
eff↓, ROS inhibition by antioxidants effectively improved MAPKs and PI3K/AKT functions and cell viability, indicating that NB enhanced cisplatin-induced cell growth in a ROS-dependent manner.
Casp3↑, the activation of caspase −3, −7, and −9 was further enhanced after the combination of 40 µg/mL of NB
Casp7↑,
Casp9↑,

739-

Bor,

Borax regulates iron chaperone- and autophagy-mediated ferroptosis pathway in glioblastoma cells

in-vitro,

GBM,

U87MG

in-vitro,

Nor,

HMC3

this report calls HMC3 "normal cells"

TumCG↓,
TumCP↓,
TumCCA↑, remarkably reduced S phase in the U87-MG cells (opposite on normal cells)
PCBP1↓,
GSH↓,
GPx4↓,
Beclin-1↑,
MDA↑,
ACSL4↑,
Casp3↑,
Casp7↑,
Ferroptosis↑,
*toxicity↓, exhibited selectivity by having an opposite effect on normal cells (HMC3).

738-

Bor,

Borax induces ferroptosis of glioblastoma by targeting HSPA5/NRF2/GPx4/GSH pathways

in-vitro,

GBM,

U251

in-vitro,

GBM,

A172

in-vitro,

Nor,

SVGp12

TumCP↓,
GPx4↓, borax treatment decreased GPx4, GSH, HSPA5 and NRF2 levels in U251 and A172 cells while increasing MDA levels and caspase‐3/7 activity.
GSH↓,
HSP70/HSPA5↓,
NRF2↓,
MDA↑,
Casp3↑,
Casp7↑,
Ferroptosis↑, Consequently, borax may induce ferroptosis in GBM cells
selectivity↑, Treating SVG cells with borax concentrations ranging from 0 to 800 μM for 24 h did not result in a significant reduction in viability compared to the control group

1652-

CA,

Caffeic Acid and Diseases—Mechanisms of Action

Review,

Var,

Dose∅, Black chokeberries seem to be the most potent source of caffeic acid (645 mg/100 g of dry weight)
ROS⇅, Therefore, we will mention the antioxidant (and prooxidant) effects of caffeic acid only briefly
NF-kB↓, In HepG2 cells, caffeic acid (100 µM) inhibited the activity of NF-κB/IL-6/STAT3 signaling, which decreased the expression of VEGF
STAT3↓,
VEGF↓,
MMP9↓, inhibited another downstream product of NF-κB: matrix metalloproteinase 9 (MM-9), which promotes tumor invasiveness and metastases
HSP70/HSPA5↑, caffeic acid (20 μM) also decreased the expression of mortalin(mitochondrial 70 kDa heat shock protein),
AST↝, normalized levels of alanine transaminase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bile acid, total cholesterol, HDL and LD
ALAT↝,
ALP↝,
Hif1a↓,
IL6↓,
IGF-1R↓,
P21↑,
iNOS↓,
ERK↓,
Snail↓,
BID↑,
BAX↑,
Casp3↑,
Casp7↑,
Casp9↑,
cycD1/CCND1↓,
Vim↓,
β-catenin/ZEB1↓,
COX2/PTGS2↓,
ROS↑, the chelating ability of caffeic acid is also responsible for its occasional pro-oxidant ability. After chelating Cu2+, the Cu2+ can be reduced to Cu+. combination of caffeic acid and endogenous copper ions can result in oxidative damage

5894-

CAR,

Targeting Gastrointestinal Cancers with Carvacrol: Mechanistic Insights and Therapeutic Potential

Review,

Var,

AntiCan↑, Carvacrol has demonstrated strong anticancer properties by modulating multiple molecular pathways governing apoptosis, inflammation, angiogenesis, and metastasis.
Apoptosis↑,
Inflam↓,
angioG↓,
TumMeta↓,
selectivity↑, revealed its ability to selectively target cancer cells while sparing healthy tissue
BioAv↑, nanotechnology have further enhanced its pharmacological profile by improving solubility, stability, and tumor-targeted delivery.
ChemoSen↑, synergistic effects when used in combination with conventional chemotherapeutics.
Dose↝, 84.38% of OEO’s contents are ‘carvacrol’.
TumCP↓, limit metastasis, induce apoptosis, suppress tumor cell proliferation, and improve the effectiveness of traditional chemotherapy medications
hepatoP↑, Carvacrol shows biological activities, such as antimicrobial, antitumor, antimutagenic, antigenotoxic, anti-inflammatory, anti-angiogenic, hepatoprotective, and antihepatotoxic properties.
Casp3↑, induced apoptosis by activating caspase-3 and caspase-9 while downregulating Bcl-2 mRNA levels
Casp9↑,
Bcl-2↓,
ROS↑, carvacrol causes oxidative stress by increasing the production of reactive oxygen species (ROS) and depleting GSH levels, which results in strong lethal effects on AGS gastric cancer
GSH↓,
BAX↑, upregulating pro-apoptotic markers such as Bax, caspase-3, caspase-7, caspase-8, caspase-9, cytochrome C, Fas, Fas-associated death domain (FADD), and p53
Casp7↑,
Casp8↑,
Cyt‑c↑,
Fas↑,
FADD↑,
P53↑,
Bcl-2↓, downregulating anti-apoptotic Bcl-2.
TumMeta↓, preventing metastasis by limiting the migration and invasion of cancer cells by upregulating epithelial markers like E-Cadherin and tissue inhibitors of metalloproteinases 2 and 3 (TIMP2 and TIMP3)
TumCMig↓,
TumCI↓,
E-cadherin↑,
TIMP2↑,
TIMP3↑,
N-cadherin↓, downregulating mesenchymal markers like N-Cadherin and ZEB2
ZEB2↓,
*lipid-P↓, protects the liver from diethylnitrosamine (DEN)-induced hepatocellular carcinogenesis by reducing lipid peroxidation, restoring key liver enzymes (AST, ALT, ALP, LDH, cGT)
*AST↓,
*ALAT↓,
*ALP↓,
*LDH↓,
*SOD↑, and enhancing antioxidant defenses (SOD, CAT, GPx, GR, GSH)
*Catalase↑,
*GPx↑,
*GSR↑,
selectivity↑, while selectively inducing apoptosis in cancer cells without harming normal liver tissue
cl‑PARP↑, inhibits HepG2 cancer cell growth by activating caspase-3, promoting PARP cleavage, downregulating Bcl-2, and modulating the MAPK signaling pathway by selectively reducing ERK1/2 phosphorylation while activating p38
ERK↓,
p38↑,
OS↑, rats (aged 6–8 weeks) demonstrated that carvacrol enhances sorafenib efficacy in HCC, improving survival rates, reducing tumor progression, and mitigating sorafenib-induced cardiac and hepatic toxicity.
AFP↓, carvacrol reduces serum alpha-fetoprotein (AFP) and alpha-L-fucosidase (AFU) levels by downregulating COX-2 and oxidative stress, inhibits angiogenesis via VEGF suppression,
COX2/PTGS2↓,
VEGF↓,
PCNA↓, prevents tumor proliferation by downregulating proliferating cell nuclear antigen (PCNA) and Ki-67 through TNF-α suppression.
Ki-67↓,
TNF-α↓,
BioAv↓, Despite carvacrol’s promising effects in vitro and in vivo, limitations such as bioavailability and solubility challenge its therapeutic application.

5919-

Cats,

Cisplatin,

Uncaria tomentosa Leaves Decoction Modulates Differently ROS Production in Cancer and Normal Cells, and Effects Cisplatin Cytotoxicity

in-vitro,

Liver,

HepG2

580 µg/mL

ROS↑, The extract increased ROS production in HepG2 cells, which resulted in decreased GSH level, leading to apoptosis of these cells through activation of caspase-3 and caspase-7
GSH↓,
Apoptosis↑,
Casp3↑,
Casp7↑,
NF-kB↓, A reduction of NF-κB active form was observed in cancer cells
selectivity↑, In normal cells the extract did not affect ROS production, GSH level and NF-κB activity, and maintained cell viability.
ChemoSen↑, enhanced cytotoxicity of CDDP against cancer cells and at the same time increased normal healthy cells resistance to cisplatin.
chemoP↑,

6124-

CHr,

EGCG,

The anticancer flavonoid chrysin induces the unfolded protein response in hepatoma cells

in-vitro,

HCC,

HepG2

TumCG↓, report that chrysin inhibits hepatoma cells growth and induces apoptosis in a dose-dependent manner.
Apoptosis↓,
GRP78/BiP↑, Chrysin induces GRP78 overexpression, X-box binding protein-1 splicing and eukaryotic initiation factor 2α phosphorylation, hallmarks of the unfolded protein response.
eff↑, GRP78 knockdown potentiates chrysin-induced caspase-7 cleavage in hepatoma cells and enhances chrysin-induced apoptosis.
cl‑Casp7↑,
cl‑PARP↑, Combination of EGCG potentiates chrysin-induced caspase-7 and poly (ADP-ribose) polymerase (PARP) cleavage.
eff↑, Finally, EGCG sensitizes hepatoma cells to chrysin through caspase-mediated apoptosis
UPR↑, data suggest that chrysin triggers the unfolded protein response. Chrysin induces the unfolded protein response
ER Stress↑, Chrysin can induce ER stress response in hepatoma cells, including up-regulation of GRP78 expression, induction of eIF-2α phosphorylation and XBP-1 splicing.
p‑eIF2α↑,
XBP-1↝,
Proteasome↓, Chrysin is a known proteasome inhibitor [27]

2805-

CHr,

Chrysin serves as a novel inhibitor of DGKα/FAK interaction to suppress the malignancy of esophageal squamous cell carcinoma (ESCC)

in-vitro,

ESCC,

KYSE150

in-vivo,

ESCC,

FAK↓, chrysin significantly disrupted the DGKα/FAK signalosome to inhibit FAK-controlled signaling pathways and the malignant progression of ESCC cells both in vitro and in vivo
GlucoseCon↓, Chrysin significantly reduced the levels of glycolytic indexes, such as glucose uptake
Casp3↑, hrysin dose-dependently increased the apoptotic rate and caspase 3/7 activity in KYSE410, KYSE30, and KYSE150 cells.
Casp7↑,
p‑Akt↓, chrysin dose-dependently inhibited the phosphorylation of AKT
TumCG↓, chrysin dose-dependently reduced the growth of ESCC tumors
Weight∅, difference of body weight between chrysin treatment groups and control group is minimal

1145-

CHr,

Chrysin inhibits propagation of HeLa cells by attenuating cell survival and inducing apoptotic pathways

in-vitro,

Cerv,

HeLa

tumCV↓,
BAX↑,
BID↑,
BOK↑,
APAF1↑,
TNF-α↑,
FasL↑,
Fas↑,
FADD↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
Mcl-1↓,
NAIP↓,
Bcl-2↓,
CDK4↓,
CycB/CCNB1↓,
cycD1/CCND1↓,
cycE1↓,
TRAIL↑,
p‑Akt↓,
Akt↓,
mTOR↓,
PDK1↓,
BAD↓,
GSK‐3β↑,
AMPK↑, AMPKa
p27/CDKN1B↑,
P53↑,

6165-

Cin,

doxoR,

Cinnamaldehyde potentiates cytotoxic and apoptogenic effects of doxorubicin in prostate cancer cell line

in-vitro,

Pca,

PC3

ChemoSen↑, current study concluded that the combination of CIN and DOX could lead to the production of a potential therapeutic agent for prostate cancer.
ROS↑, CIN-enhanced DOX potency resulted from increasing ROS generation
Casp3↑, adding CIN at the concentrations of 25 and 50 μg/mL to DOX could significantly potentiate the DOX anti-tumor effect on the activation of caspase-3/7
Casp7↑,

6162-

Cin,

Anticancer Potential and Molecular Mechanisms of Cinnamaldehyde and Its Congeners Present in the Cinnamon Plant

Review,

Var,

AntiCan↑, Cinnamaldehyde and its congeners have shown their ability to act against several cancers.
Apoptosis↑, graphical abstract
ROS↑,
BAX↑,
Cyt‑c↑,
Fas↑,
Casp9↑,
E-cadherin↑,
Casp7↑,
PARP↑,
Bak↑,
AMPK↑,
Ca+2↑,
BAD↑,
MMP↓,
cycA1/CCNA1↓,
CycB/CCNB1↓,
ERK↓,
VEGF↓,
TumCP↓,
MAPK↓,
mTOR↓,
PI3K↓,
PCNA↓,
Bcl-2↓,
TumCCA↑, Some of the mechanistic approaches include the induction of apoptosis, cell cycle arrest, interruption in angiogenesis, free radical scavenging, inhibition of inflammation, and interference with cellular invasion and metastasis.
angioG↓,
*ROS↓,
Inflam↓,

6202-

Cuc,

Cucurbitacins as potential anticancer agents: new insights on molecular mechanisms

Review,

Var,

*Inflam↓, anti-inflammatory, antioxidant, antimalarial, antimicrobial, hepatoprotective and antitumor potential.
*antiOx↑,
*hepatoP↑,
AntiTum↑,
AntiCan↑, important anticancer/chemopreventive potential
*chemoPv↑,
*AntiDiabetic↑, antidiabetic, hepatoprotective, and immunomodulator
*Imm↑,
Hif1a↓, for gastric cancer, cucurbitacin B reversed the multi-drug resistance of the SGC7901/DDP gastric cancer cells by downregulating the drug-resistant protein HIF-1a and P-pg.
P-gp/ABCB1↓,
mTORC1↓, cucurbitacin B induced apoptosis and autophagy by inhibiting mTORC1.
ERK↓, by inactivating the extracellular signal-regulated kinase (ERK) 1/2, p38, and the Akt signaling pathway [61].
Akt↓,
Casp3↑, substantial increase in the activity of Caspase 3/7 in the human prostate cancer cell lines LNCaP and PC-3,
Casp7↑,
ATP↓, authors proposed cucurbitacin’s dose-dependent inhibition of ATP citrate lyase, or ACYL, as the anticancer mechanism of cucurbitacin, in in vitro and in vivo prostate tumour models
RadioS↑, cucurbitacin B combined with ionizing radiation blocks cancer cells in the G2/M phase and promotes apoptosis, inhibiting cancer cells.
ChemoSen↑, cucurbitacin B exhibited cytotoxicity against the ovarian cancer cell line A2780, and pretreatment of cisplatin-resistant cell line A2780CP with this natural compound led to a significant increase in the cytotoxicity of cisplatin

6686-

DAP,

Lactoferrin-encapsulated dichloroacetophenone (DAP) nanoparticles enhance drug delivery and anti-tumor efficacy in prostate cancer

in-vivo,

Pca,

mouse

PDK1↓, pplication of 2,2-dichloroacetophenone (DAP), a PDK1 inhibitor,
TumCP↓, In this study we demonstrated that DAP exhibited a superior ability to inhibit prostate cancer cell proliferation, migration and colony formation at a lower concentration (20 μM) compared to a previously established inhibitor, dichloroacetate (DCA),
TumCMig↓,
BioAv↓, However, poor aqueous solubility and lower stability of DAP limits its therapeutic application
BioAv↑, Nano formulation of DAP with natural lactoferrin enhanced its dispersion and stability by increasing polydispersity index and intensity, and reduced zeta potential values upon conjugation that overcame the solubility limitations of DAP.
Apoptosis↑, these nanoparticles induce apoptosis in cancer cells by inducing caspase3/7 activity and disrupting the glycolytic and oxidative phosphorylation pathways.
Casp3↑,
Casp7↑,
Glycolysis↓,

6607-

Ech,

Cytotoxic effects of Echinacea root hexanic extracts on human cancer cell lines

in-vitro,

PC,

MIA PaCa-2

in-vitro,

CRC,

Colo320

tumCV↓, all the three species reduced cell viability in a concentration- and time-dependent manner
eff↑, Echinacea pallida was the most active species with IC(50)s of 46.41+/-0.87 and 10.55+/-0.70 microg/ml in MIA PaCa-2 and COLO320 cells, respectively.
Apoptosis↑, Echinacea pallida extract was able to induce apoptosis by increasing significantly caspase 3/7 activity and promoting nuclear DNA fragmentation.
Casp3↑,
Casp7↑,
DNAdam↑,
Imm↑, A possible efficacy of Echinacea extracts in anticancer therapy has been related to their well documented immunostimulatory activities due to high molecular weight polysaccharides
NK cell↑, such an effect has been ascribed to natural killer (NK) cell stimulation and inhibition of the endogenous suppressors of NK cells (i.e., the prostaglandins)
PGE2↓,
COX1↓, Nonetheless, Echinacea alkylamides showed to inhibit cyclooxygenase-1 and -2 (COX-1 and COX-2) and 5-lipooxygenase
COX2/PTGS2↓,
5LO↓,

6620-

Ech,

Echinacea purpurea diminishes neovascular reaction induced in mice skin by human cancer cells and stimulates non-specific cellular immunity in humans

in-vivo,

Var,

mice

angioG↓, Echinacea preparation caused inhibition of angiogenesis induced by human lung and kidney cancer cells
*NK cell↑, increased the incidence of CD16 + and CD56+ NK cells in their blood.
Imm↑, Echinacea purpurea belongs to the most important herbal remedies with immunostimulatory properties
Inflam↓, Echinacea extracts contain many compounds with immunomodulatory and anti-inflammatory activity – alkamides, polysaccharides, polyphenols, glycoproteins, essential oils, tannins, and others
tumCV↓, In in vitro studies Echinacea reduced human cancer cells viability [5].
Apoptosis↑, Chicca et al described that E. pallida extract was able to induce apoptosis of human pancreatic cancer and colon cancer cell lines by increasing significantly caspase 3/7 activity and promoting nuclear DNA fragmentation [5].
Casp3↑,
Casp7↑,
DNAdam↑,
MMPs↓, flavonoids, present also in Echinacea extract, inhibit activities of metalloproteinases
other↑, E. purpurea might be effective in reducing chemotherapy-induced leukopenia in patients with advanced gastric cancer [

3208-

EGCG,

Induction of Endoplasmic Reticulum Stress Pathway by Green Tea Epigallocatechin-3-Gallate (EGCG) in Colorectal Cancer Cells: Activation of PERK/p-eIF2α/ATF4 and IRE1α

in-vitro,

Colon,

HT29

in-vitro,

Nor,

3T3

TumCD↓, EGCG treatment was toxic to the HT-29 cell line
ER Stress↑, EGCG induced ER stress in HT-29 by upregulating immunoglobulin-binding (BiP), PKR-like endoplasmic reticulum kinase (PERK), phosphorylation of eukaryotic initiation factor 2 alpha subunit (eIF2α), activating transcription 4 (ATF4), and IRE1α
GRP78/BiP↑,
PERK↑,
eIF2α↑,
ATF4↑,
IRE1↑,
Apoptosis↑, Apoptosis was induced in HT-29 cells after the EGCG treatment, as shown by the Caspase 3/7 activity.
Casp3↑,
Casp7↑,
Wnt↓, (CRC) via suppression of the Wnt/β-catenin pathway
β-catenin/ZEB1↓,
*toxicity∅, This embryonic fibroblast cell line (3T3) has shown that the EGCG was not toxic to normal healthy cells, given the treatment at any concentration even at the highest concentration of EGCG (1000 μM).
UPR↑, ER stress is induced by EGCG and activates UPR proteins

26-

EGCG,

QC,

docx,

Green tea and quercetin sensitize PC-3 xenograft prostate tumors to docetaxel chemotherapy

vitro+vivo,

Pca,

PC3

BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,

22-

EGCG,

Inhibition of sonic hedgehog pathway and pluripotency maintaining factors regulate human pancreatic cancer stem cell characteristics

in-vitro,

PC,

CD133+

in-vitro,

PC,

CD44+

in-vitro,

PC,

CD24+

in-vitro,

PC,

ESA+

 20-60 uM

HH↓, EGCG also inhibited the components of Shh pathway (smoothened, patched, Gli1 and Gli2)
Smo↓,
PTCH1↓,
PTCH2↓,
Gli1↓,
GLI2↓,
Gli↓,
Bcl-2↓, inhibiting the expression of Bcl-2 and XIAP, and activating caspase-3
XIAP↓,
Shh↓,
survivin↓,
Casp3↑,
Casp7↑,
CSCs↓, EGCG inhibited the expression of pluripotency maintaining transcription factors (Nanog, c-Myc and Oct-4), and self-renewal capacity of pancreatic CSCs.
Nanog↓,
cMyc↓,
OCT4↓,
EMT↓, EGCG inhibited EMT by inhibiting the expression of Snail, Slug and ZEB1, and TCF/LEF transcriptional activity,
Snail↓,
Slug↓,
Zeb1↓,
TumCMig↓, significantly reduced CSC’s migration and invasion, suggesting the blockade of signaling involved in early metastasis.
TumCI↓,
eff↑, combination of quercetin with EGCG had synergistic inhibitory effects on self-renewal capacity of CSCs through attenuation of TCF/LEF and Gli activities

6836-

EMD,

Emodin and the Anthraquinone Scaffold: Therapeutic Promise and Strategies to Overcome Translational Barriers

Review,

Nor,

*antiOx↑, graphic abstract
*neuroP↑,
*Inflam↓,
*hepatoP↑,
AntiTum↑,
*Bacteria↓,
*diuretic↑,
*AntiDiabetic↑,
*BioAv↝, formulation composition and herb–herb or herb–drug interactions are critical determinants of anthraquinone bioavailability and, ultimately, therapeutic outcomes.
*NF-kB↓, figure 4
*AMPK↑,
*JAK↓,
*STAT3↓,
*ROS↓, At low to moderate concentrations, particularly in models of inflammatory or oxidative tissue injury, emodin exerts net antioxidant and cytoprotective effects by lowering ROS levels, limiting lipid peroxidation, and enhancing endogenous antioxidant d
*lipid-P↓,
ROS↑, in cancer cells and other metabolically stressed conditions, the anthraquinone scaffold has been reported to act predominantly as a pro-oxidant, shifting redox homeostasis toward oxidative stress and promoting intracellular ROS accumulation,
TumCCA↑, In human colon cancer (WiDr) cells, aloe-emodin induced a pronounced G2/M arrest associated with suppression of cyclin B1, a critical regulator of mitotic entry.
CycB/CCNB1↓,
BAX↑, upregulation of Bax and Bak alongside the downregulation of anti-apoptotic members such as Bcl-2 and Bcl-xL.
Bcl-2↓,
MOMP↑, As a result, mitochondrial outer-membrane permeabilization (MOMP) is promoted, enabling cytochrome c release and subsequent apoptosome formation through association with Apaf-1.
Cyt‑c↑,
Casp9↑, Activation of initiator caspase-9 follows, triggering executioner caspases, notably caspase-3 and caspase-7, and culminating in apoptotic cell death
Casp3↑,
Casp7↑,
Apoptosis↑,
P53↑, where emodin-induced ROS accumulation and p53 activation contribute to the inhibition of pathological proliferation relevant to restenosis and atherosclerotic remodeling

6584-

EU,

Eurycoma longifolia: an overview on the pharmacological properties for the treatment of common cancer

Review,

Var,

*AntiAge↑, he aqueous extract and decoction made from its root have been shown to enhance fertility, sexual activity and possess anti-aging properties.
*Inflam↓, he anti-malarial, anti-inflammatory, anti-oxidant and anti-microbial are the most common activities exerted by this plant.
*antiOx↑,
TumCD↑, Initially, eurycomanone is reported to induce cell death via down regulating of Bcl-2 protein together with cleavage of protein caspase-7 and PARP-1.
Bcl-2↓,
cl‑Casp7↑,
cl‑PARP↑,
BAX↑, increase of the proteins bax and p53, as well as the inhibition of the protein Bcl-2, in a number of cancer cells.
P53↑,
tumCV↓, Treatment on malignant cells with eurycomanone including (HeLa, CaOv, HepG2, MCF7, HM3KO) cell lines greatly decreases quantity of viable cells.
selectivity↑, It is also found that the eurycomanone is relatively benign to non-cancer cell lines (i.e. Vero, MDBK)
*testos↑, It also mentioned E. longifolia extract raises serum testosterone levels, there may be a danger risk associated with its use in older men because it could result in prostatic issues.
*PSA∅, no change in serum levels of prostate-specific antigen (PSA) between the verum and placebo groups.

6332-

Eug,

Anti-metastatic and anti-proliferative activity of eugenol against triple negative and HER2 positive breast cancer cells

in-vitro,

BC,

MDA-MB-231

in-vitro,

BC,

SkBr3

TumCP↓, Treatment with 4 μM and 8 μM eugenol for 48 h significantly inhibited cell proliferation of MDA-MB-231, with an inhibition rate of 76.4%,
MMP2↓, Eugenol-treated cells showed significantly decreased MMP2 and MMP9 expression and an insignificant increase in TIMP1 expression in HER2 positive and triple negative breast cancer cells.
MMP9↓,
TIMP1↑,
Apoptosis↑, late apoptosis and increased the expression of Caspase3, Caspase7, and Caspase9.
Casp3↑,
Casp7↑,
Casp9↑,

6858-

FBZ,

Fenbendazole and Diisopropylamine Dichloroacetate Exert Synergistic Anti-cancer Effects by Inducing Apoptosis and Arresting the Cell Cycle in A549 Lung Cancer Cells

in-vitro,

Lung,

A549

eff↑, The combination of FZ and DADA exhibited a synergistic effect on inhibiting the proliferation of A549 lung cancer cells.
mt-ROS↑, After 48 h of treatment, the FZ-DADA combination produced reactive oxygen species (ROS) and promoted apoptosis by down-regulating Bcl2 and up-regulating BAX protein expression.
Apoptosis↑, The combination modulates key apoptotic proteins, induces cell cycle arrest, and increases mitochondrial ROS production
Bcl-2↓,
BAX↑,
Casp3↑, The combination activated caspase-3, caspase-7, and PARP, further driving apoptosis in A549 cells
Casp7↑,
PARP↑,
TumCCA↑, The FZ-DADA treatment also induced cell cycle arrest, as evidenced by the inhibition of Cyclin A and Cyclin E proteins.
cycA1/CCNA1↓,
cycE/CCNE↓,

2859-

FIS,

The Natural Flavonoid Fisetin Inhibits Cellular Proliferation of Hepatic, Colorectal, and Pancreatic Cancer Cells through Modulation of Multiple Signaling Pathways

in-vitro,

Liver,

HepG2

3.2μM

NA,

Colon,

Caco-2

16.4 μM

TumCG↓, fisetin induces growth inhibition, and apoptosis in hepatic (HepG-2), colorectal (Caco-2) and pancreatic (Suit-2) cancer cell lines.
other↝, activation of CDKN1A, SEMA3E, GADD45B and GADD45A and down-regulation of TOP2A, KIF20A, CCNB2 and CCNB1 genes.
Casp3↑, Fisetin caused significant increase in activation of caspase 3/7 compared to untreated control
Casp7↑,
PGE2↓, Fisetin inhibits PGE2 production
GSTs↓, GST enzyme activity assay has been carried out. The results showed that fisetin induced enzyme inhibition in a dose dependent manner
Wnt↓, inhibiting Wnt/EGFR/NF-kB and COX-2 signaling pathways
EGFR↓,
NF-kB↓,
COX2/PTGS2↓,
P53↑, induction of p53 and p21
P21↑,
P450↓, Fisetin also was able to inhibit cyctochrome P450 (CYP450 3A4) and glutatihione -S-transferase activity

2824-

FIS,

Fisetin in Cancer: Attributes, Developmental Aspects, and Nanotherapeutics

Review,

Var,

*antiOx↑, Fisetin is one such naturally derived flavone that offers numerous pharmacological benefits, i.e., antioxidant, anti-inflammatory, antiangiogenic, and anticancer properties.
*Inflam↓,
angioG↓,
BioAv↓, poor bioavailability associated with its extreme hydrophobicity hampers its clinical utility
BioAv↑, The issues related to fisetin delivery can be addressed by adapting to the developmental aspects of nanomedicines, such as formulating it into lipid or polymer-based systems, including nanocochleates and liposomes
TumCP↓, fisetin also inhibits tumor proliferation by repressing tumor mass multiplication, invasion, migration, and autophagy.
TumCI↓,
TumCMig↓,
*neuroP↑, figure 2
EMT↓, It affects the cell cycle and thereby cell proliferation, microtubule assembly, cell migration and invasion, epithelial to mesenchymal transition (EMT), and cell death
ROS↑, cell death caused by fisetin is possibly due to the induction of apoptosis by fisetin or other signaling molecules and reactive oxygen species (ROS)
selectivity↑, Without influencing the growth of normal cells, fisetin has the capability to hinder the formation of colonies and inhibit the multiplication of cancer cells.
EGFR↓, fisetin restricts the multiplication of EGFR 2-overexpressing SK-BR-3 breast tumor masses
NF-kB↓, fisetin inhibits cancer metastasis by reducing the expressions of nuclear factor-kB (NF-kB)-modulated metastatic proteins in a variety of tumor cell types, including vascular endothelial growth factor (VEGF) and matrix metalloproteinase-9 (MMP)
VEGF↓,
MMP9↓,
MMP↓, rupturing the plasma membrane, depolarizing mitochondria, cleaving PARP, and activating caspase-7, -8, and -9.
cl‑PARP↑,
Casp7↑,
Casp8↑,
Casp9↑,
*ROS↓, Fisetin is a bioactive flavonol molecule that can easily penetrate the cell membrane due to its hydrophobic nature [51,52], reducing the generation of inflammatory cytokines and reactive oxygen species (ROS) in microglial cells, (normal cells)
uPA↓, Perhaps fisetin lowers angiogenesis, consequently suppressing tumor multiplication by urokinase plasminogen activator (uPA) inhibition
MMP1↓, powerful matrix metalloproteinase (MMP)-1 inhibitor
Wnt↓, Fisetin works on several cellular pathways, such as Wnt, Akt-PI3K, and ERK, as an inhibitor
Akt↓,
PI3K↓,
ERK↓,
Half-Life↝, Fisetin exhibits a very short terminal half-life of approximately 3 hrs in its free form. This half-life is found to be less than that of its metabolites

7009-

Fuc,

Effects of Fucoidan and Chemotherapeutic Agent Combinations on Malignant and Non-malignant Breast Cell Lines

in-vitro,

BC,

MCF7

in-vitro,

Nor,

MCF12A

selectivity↑, Fucoidan alone was significantly more cytotoxic to MCF-7 breast cancer cells compared to the MCF-12A non-cancerous breast epithelial cell line.
TumCCA↑, In MCF-7 cells, the presence of fucoidan caused cell cycle arrest at G1 with accumulation of cells in the sub-G1 phase with the activation of caspases-3,-7 and -9.
Casp3↑,
Casp7↑,
Casp9↑,
ChemoSen↑, combination of fucoidan with the standard chemotherapeutic agents-cisplatin, doxorubicin and taxol-significantly enhanced the cytotoxicity of these drugs and accumulation of cells in the G2/M and sub-G1 phases, and induction of apoptosis.
chemoP↑, in non-cancerous MCF-12A cells, fucoidan attenuated the toxicity of doxorubicin and cisplatin in combination by increasing their IC50 values.

7006-

Fuc,

Seaweeds in the Oncology Arena: Anti-Cancer Potential of Fucoidan as a Drug—A Review

Review,

Var,

*toxicity↓, Fucoidan is a versatile, nontoxic marine-origin heteropolysaccharide that has received much attention due to its beneficial biological properties and safety.
*AntiViral↑, ucoidan has been demonstrated to exhibit a variety of conventional bioactivities, such as antiviral, antioxidant, and immune-modulatory characteristics, and anticancer activity against a wide range of malignancies has also recently been discovered.
*antiOx↑,
*Imm⇅,
AntiCan↑,
TumCCA↑, Fucoidan inhibits tumorigenesis by prompting cell cycle arrest and apoptosis, blocking metastasis and angiogenesis, and modulating physiological signaling molecules.
Apoptosis↑,
TumMeta↓,
angioG↓,
antiNeop↑, Fucoidans’ capacity to bind to Toll-like receptors and intervene with the action of vascular endothelial growth factors (VEGF) and matrix metalloproteinases (MMPs) could explain their anti-neoplastic properties
VEGF↓,
MMPs↓,
BioAv↑, Low molecular weight fractions (LMWF), in particular, are thought to be more biocompatible [47]
BioAv↑, in rats, following topical administration of fucoidan (MW 750 kDa) from Fucus vesiculosus demonstrated fine skin-penetrating characteristics.
ROS⇅, Induction/inhibition of reactive oxygen species (ROS), mitochondrial instability, and caspase and poly (ADP-ribose) polymerase (PARP) cleavage are all aspects of it
cl‑PARP↑, fucoidan treatment causes PARP cleavage and caspase-3/7 activation in MCF-7 cells, which are hallmarks of apoptosis [
Casp3↑,
Casp7↑,
ROS↑, human hepatoma SMMC-7721 cells, fucoidan therapy caused noteworthy growth inhibition and ROS-mediated apoptosi
GSH↓, lower glutathione consumption (GSH), mitochondrial swelling, and depolarization of the mitochondrial membrane potential
MMP↓,
PI3K↓, Fucoidan inhibits PI3K, suppressing ERK and activates MAPK, limiting cancer cell proliferation and decreasing Bcl-2 to Bax ratio, inducing caspase-dependent apoptosis in BEL-7402 and LM3 cell lines
ERK↓,
MAPK↑,
TumCP↓,
Bax:Bcl2↑,
TJ↑, Meanwhile, dietary fucoidan progressively restores intestinal villi by upregulating the expression of tight junction proteins such as ZO-1, Occludin, Claudin-1, and Claudin-8 via p38 MAPK and ERK1/2 activation.
ZO-1↑,
OCLN↑,
CLDN1↑,
IBI↑, fucoidan supplementation improves intestinal barrier function by enhancing intestinal microbiota diversity
GutMicro↑,
NK cell↑, ↑NK cell-mediated anticancer immunity
STAT3↓, Inhibits STAT3 Signaling
eff↑, Astragalus polysaccharide as a topical mucosal adjuvant to boost the anticancer efficacy of immune checkpoint inhibitors

1155-

Fuc,

The anti-cancer effects of fucoidan: a review of both in vivo and in vitro investigations

Review,

NA,

100 μg/mL

*toxicity↓, Sprague–Dawley rats, researchers didn’t observe significant side effects when taking 0–1000 mg/kg fucoidan orally for 28 days.
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
VEGF↓,
angioG↓,
PI3K↓,
Akt↓,
PARP↑,
Bak↑,
BID↑,
Fas↑,
Mcl-1↓,
survivin↓,
XIAP↓,
ERK↓,
EMT↓, Fucoidan can reverse the EMT effectively
EM↑,
IM↓,
Snail↓,
Slug↓,
Twist↓,

7136-

GI,

[6]-shogaol inhibits growth and induces apoptosis of non-small cell lung cancer cells by directly regulating Akt1/2

vitro+vivo,

NSCLC,

H1650

TumCP↓, Among the compounds, [6]-shogaol showed the greatest inhibitory effects on the NSCLC cell proliferation and anchorage-independent growth.
TumCCA↑, [6]-Shogaol induced cell cycle arrest (G1 or G2/M) and apoptosis.
Apoptosis↑,
Akt↓, Furthermore, [6]-shogaol inhibited Akt kinase activity, a downstream mediator of EGFR signaling, by binding with an allosteric site of Akt.
EGFR↓,
STAT3↓, [6]-shogaol reduced the constitutive phosphorylation of signal transducer and activator of transcription-3 (STAT3) and decreased the expression of cyclin D1/3, which are target proteins in the Akt signaling pathway.
cycD1/CCND1↓,
Casp3↑, The induction of apoptosis in NCI-H1650 cells by [6]-shogaol corresponded with the cleavage of caspase-3 and caspase-7.
Casp7↑,
TumCG↓, Moreover, intraperitoneal administration of [6]-shogaol inhibited the growth of NCI-H1650 cells as tumor xenografts in nude mice.
Ki-67↓, [6]-Shogaol suppressed the expression of Ki-67, cyclin D1 and phosphorylated Akt and STAT3 and increased terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling-positivity in xenograft tumors.
eff↑, Our study revealed that [6]-shogaol is more potent than [6]-paradol or [6]-gingerol in reducing cell viability and inhibiting anchorage-independent growth of NSCLC cells.
Dose↝, treatment with 10 or 40mg/kg body weight of [6]-shogaol

841-

Gra,

The Chemopotential Effect of Annona muricata Leaves against Azoxymethane-Induced Colonic Aberrant Crypt Foci in Rats and the Apoptotic Effect of Acetogenin Annomuricin E in HT-29 Cells: A Bioassay-Guided Approach

in-vitro,

CRC,

HT-29

1.62ug/ml@48hr

in-vitro,

Nor,

CCD841

32.51μg/ml@48 h

normal human colon cells

PCNA↓,
Bcl-2↓,
BAX↑,
*MDA↓, decrease in the malondialdehyde level of the colon tissue homogenates
lipid-P↓, suggesting the suppression of lipid peroxidation
TumCG↓, G1 cell cycle arrest
MMP↓,
Cyt‑c↑, leakage of cytochrome c from the mitochondria
Casp3↑,
Casp7↑,
Casp9↑,
*ROS↓, confirmed the protective effects of EEAML against oxidative stress in colon tissues
LDH↓, irreversible membrane damage to cells causes a leakage of LDH from the cytosol
*toxicity↓, IC50: <2ug/ml for cancer, but 32ug/ml for normal cells
selectivity↑, When compared with HT-29 cells, annomuricin E was far less cytotoxic to the normal cells, as revealed by the relatively high IC50 value on CCD841 (32.51 ± 1.18 μg/ml for 48 h)

850-

Gra,

Selective cytotoxic and anti-metastatic activity in DU-145 prostate cancer cells induced by Annona muricata L. bark extract and phytochemical, annonacin

in-vitro,

PC,

PC3

0.1uM(Annonacin) 55ug/mL(EAB)

without impacting RWPE-1 normal prostate cells

in-vitro,

Pca,

DU145

ROS∅, EAB extract and annonacin does not elicit ROS generation in DU-145 cells
MMP∅,
Casp3↑, suggesting a caspase independent cell death
Casp7↑,
VEGF↓,

7359-

HibSad,

Novel Insight into the Cellular and Molecular Signalling Pathways on Cancer Preventing Effects of Hibiscus sabdariffa: A Review - PubMed

Review,

Var,

AntiCan↑, Hibiscus sabdariffa (HS) plant, including anthocyanin, flavonoids, saponins, tannins, polyphenols, organic acids, caffeic acids, citric acids, protocatechuic acid, and others, extracts of this plant have been reported to have anti-cancer effects.
TumCP↓, These compounds have been shown to reduce cancer cell proliferation, induce apoptosis, and cause cell cycle arrest.
Apoptosis↑,
TumCCA↑,
P53↑, They also increase the expression levels of the cell cycle inhibitors (p53, p21, and p27) and the pro-apoptotic proteins (BAD, Bax, caspase 3, caspase 7, caspase 8, and caspase 9).
P21↑,
p27/CDKN1B↑,
BAD↑,
BAX↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
*AntiBio↑, Anti-microbial effect
*Inflam↓, Anti-inflammatory effect
*antiOx↑, In calyces of HS, compounds such as anthocyanins have antioxidant properties
*BP↓, The tea made from the HS leaves effectively lowers the blood pressure level in patients because of the presence of phytochemicals that induce systemic vasodilation along
*AntiDiabetic↑, calyces extract of HS can reduce the blood sugar level in diabetic patients
HDAC1↓, HS extract mediated inhibitory responses which were attributed to their inhibition of histone deacetylases (HDACs), specifically HDAC1 and HDAC3.
HDAC3↓,
tumCV↓, PCA dependently decreased cell viability, increased lactate dehydrogenase (LDH) leakage, enhanced DNA fragmentation, reduced mitochondrial membrane potential
LDL↓,
DNAdam↑,
MMP↓,
*Catalase↑, Ethanolic extract of the HS substantially increases the levels of the antioxidants CAT, SOD, GPx and reduced glutathione (GSH) in brain tissue, thus possessing significant antioxidant activity.
*SOD↑,
*GPx↑,
*GSH↑,
*antiOx↑,
*ROS↓, Anthocyanin in the extract of HS acts on the anti-oxidant system, and scavenges free radicals thus reducing damage to genomes of regular cells and the mutations, thus stopping tumor formation
TumCMig↓, PCA found in extract of HS inhibited cell migration and invasion to non-cytotoxic cells via down-regulation of the Ras/Akt/NF-κβ pathway and MMP-2 production [92].
TumCI↓,
selectivity↑,
RAS↓,
Akt↓,
NF-kB↓,
MMP2↓,
PI3K↓, decreasing PI3K, P-Akt protein, MMP expression, anti-apoptotic Bcl-2, Bcl-xL proteins, and PCNA, cyclin A, D1, B1, and E.
Bcl-2↓,
Bcl-xL↓,
PCNA↓,
cycA1/CCNA1↓,
cycD1/CCND1↓,
cycE/CCNE↓,

2879-

HNK,

Honokiol Inhibits Lung Tumorigenesis through Inhibition of Mitochondrial Function

in-vitro,

Lung,

H226

in-vivo,

NA,

mouse

tumCV↓, honokiol significantly reduced the percentage of bronchial that exhibit abnormal lung SCC histology from 24.4% bronchial in control to 11.0% bronchial in honokiol treated group (p= 0.01) while protecting normal bronchial histology (present in 20.5%
selectivity↑,
TumCP↓, In vitro studies revealed that honokiol inhibited lung SCC cells proliferation, arrested cells at the G1/S cell cycle checkpoint, while also leading to increased apoptosis.
TumCCA↑,
Apoptosis↑,
mt-ROS↑, interfering with mitochondrial respiration is a novel mechanism by which honokiol increased generation of reactive oxygen species (ROS) in the mitochondria, : mitochondrial ROS generation
Casp3↑, cells treated with honokiol showed a significant increase in caspase 3/7 activity, which occurred in dose- and time-dependent manners
Casp7↑,
OCR↓, Honokiol caused a fast and concentration-dependent decrease in basal oxygen consumption rate (OCR) in both cell lines
Cyt‑c↑, cytochrome c release was increased in honokil treated mouse lung SCC tissue
ATP↓, found a dramatic decrease in cellular ATP content
mitResp↓, Honokiol inhibits mitochondrial respiration and decreases ATP levels in H226 and H520 cells, which may elevate AMP and the intracellular AMP/ATP ratio, leading to activation of the AMPK
AMP↑,
AMPK↑,

7655-

IP,

SFN,

Combined Phytochemical Sulforaphane and Dietary Fiber Inulin Contribute to the Prevention of ER-Negative Breast Cancer via PI3K/AKT/MTOR Pathway and Modulating Gut Microbial Composition

in-vivo,

BC,

mice

Dose↝, Transgenic mice representing estrogen receptor-negative BC were fed 26% (w/w) BSp and 2% (w/v) inulin supplemented in food and water, respectively. The amount of BSp consumed by a mouse is equivalent to a daily intake of 234 g of BSp for an adult
TumCG↓, combinatorial treatment inhibited tumor growth, increased tumor onset latency, and synergistically reduced tumor weight.
TumW↓,
GutMicro↑, Ruminococcus, Muribaculaceae, and Faecalibaculum significantly increased, while Blautia, Turicibacter, and Clostridium sensu stricto 1 significantly decreased in the combinatorial group compared with the control group
HDAC↓, combinatorial treatment induced a protective epigenetic effect by inhibiting histone deacetylases (HDACs) and DNA methyltransferases (DNMTs).
DNMTs↓,
Akt↓, Intermediates in the AKT/PI3K/MTOR pathway were significantly suppressed by the combinatorial treatment, including PI3K p85, p-AKT, p-PI3K p55, MTOR, and NF-κB.
PI3K↓,
mTOR↓,
NF-kB↓,
TumCCA↑, Cell cycle arrest and programmed cell death were induced by the combinatorial treatment via elevating the expression of cleaved-caspase 3 and 7 and inhibiting the expressions of CDK2 and CDK4, respectively
cl‑Casp3↑,
cl‑Casp7↑,
CDK2↓,
CDK4↓,
Risk↓, Overall, the findings suggest that early-life dietary combinatorial treatment contributed to BC prevention
Dose↝, The dosage of inulin used in this experiment was lower than that used in a previous study, which suggested that 8% (w/v) inulin, equivalent to 40 g of fiber per day, is physiologically achievable and practical for human patients

7747-

ISL,

Isoliquiritigenin Induces Apoptosis via ROS-Mediated Inhibition of p38/mTOR/STAT3 Pathway in Human Melanoma Cells

in-vitro,

Melanoma,

SK-MEL-28

*Inflam↓, Isoliquiritigenin (ISL), a phenolic compound derived from licorice, exhibits various biological activities, including anti-inflammatory, anti-viral, anti-tumor, and antioxidant effects
*AntiViral↑,
*AntiTum↑,
*antiOx↑,
cl‑Casp9↑, ISL treatment induces apoptosis in SK-MEL-28 cells, as evidenced by the cleavage of caspase-9, -7, -3, and PARP.
cl‑Casp7↑,
cl‑Casp3↑,
cl‑PARP↑,
BAX↑, ISL increased Bax expression, decreased Bcl-2 expression, and promoted cytochrome C release into the cytosol.
Bcl-2↓,
Cyt‑c↑,
cycD1/CCND1↓, ISL also reduced the expression of cell cycle markers, including cyclin D1, D3, and survivin.
cycD1/CCND1↓,
survivin↓,
ROS↓, Notably, ISL treatment markedly increased intracellular ROS levels
eff↓, pretreatment with N-acetyl cysteine(NAC), a ROS scavenger, abrogated the ISL-induced inhibition of the p38/mTOR/STAT3 pathway and prevented apoptosis.
p‑mTOR↓, ISL significantly diminished the constitutive phosphorylation of mTOR and STAT3 in SK-MEL-28 cells by blocking the phosphorylation of p38 MAPK
p‑STAT3↓,
p‑MAPK↓,

Showing Research Papers: 1 to 50 of 83
Page 1 of 2 Next

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 83

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,
Total Targets: 264

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1, CD19↑, 1, diuretic↑, 1,

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 11, Catalase↑, 4, GPx↑, 4, GSH↑, 2, GSR↑, 1, GSTs↑, 1, HDL↑, 1, lipid-P↓, 4, MDA↓, 2, ROS↓, 8, SOD↑, 4,

Core Metabolism/Glycolysis(tgid=4) ⓘ

ALAT↓, 1, AMPK↑, 1, HMG-CoA↓, 1, LDH↓, 1, LDL↓, 1,

Cell Death(tgid=5) ⓘ

Akt↓, 1, BAX↓, 1, iNOS↓, 2, MAPK↓, 1,

Transcription & Epigenetics(tgid=7) ⓘ

cJun↓, 1,

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

PI3K↓, 1, STAT3↓, 1,

Migration(tgid=13) ⓘ

AP-1↓, 1, PKCδ↓, 1,

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1, VEGF↓, 1,

Barriers & Transport(tgid=15) ⓘ

GastroP↑, 1,

Immune & Inflammatory Signaling(tgid=16) ⓘ

CD4+↑, 1, COX2/PTGS2↓, 3, CRP↓, 1, IL10↑, 1, IL6↓, 1, Imm↑, 1, Imm⇅, 1, Inflam↓, 10, JAK↓, 1, NF-kB↓, 2, NK cell↑, 2, PSA∅, 1, TNF-α↓, 1,

Hormonal & Nuclear Receptors(tgid=20) ⓘ

testos↑, 1,

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↝, 1, Dose↝, 2, P450↓, 1,

Clinical Biomarkers(tgid=22) ⓘ

ALAT↓, 1, ALP↓, 1, AST↓, 1, BP↓, 1, CRP↓, 1, IL6↓, 1, LDH↓, 1, PSA∅, 1, TG/TAG↓, 1,

Functional Outcomes(tgid=23) ⓘ

AntiAge↑, 1, AntiCan↑, 1, AntiDiabetic↑, 4, AntiTum↑, 1, cardioP↑, 2, chemoPv↑, 1, hepatoP↑, 3, neuroP↑, 5, toxicity↓, 4, toxicity∅, 1,

Infection & Microbiome(tgid=24) ⓘ

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

Scientific Paper Hit Count for: Casp7, Caspase-7

6 EGCG (Epigallocatechin Gallate)
6 Thymoquinone
5 Quercetin
5 Sulforaphane (mainly Broccoli)
5 Magnetic Fields
4 Silver-NanoParticles
3 Cisplatin
3 Chrysin
3 Fucoidan
2 Phyllanthus emblica/Emblica officinalis/Amla / Indian Gooseberry
2 Apigenin (mainly Parsley)
2 Berberine
2 Betulinic acid
2 Boron
2 Cinnamon
2 Echinacea
2 Fisetin
2 Graviola
2 Phenylbutyrate
2 Piperlongumine
1 Auranofin
1 Baicalein
1 Biochanin A
1 Beta-Caryophyllene
1 Bromelain
1 borneol
1 Caffeic acid
1 Carvacrol
1 Cat’s Claw
1 doxorubicin
1 Cucurbitacin
1 Dichloroacetophenone(2,2-)
1 Docetaxel
1 Emodin
1 Eurycomanone
1 Eugenol
1 Fenbendazole
1 Ginger/6-Shogaol/Gingerol
1 Hibiscus sabdariffa
1 Honokiol
1 Inulin Prebiotic
1 Isoliquiritigenin
1 Luteolin
1 Lycopene
1 Iron
1 Chemotherapy
1 Magnetic Field Rotating
1 Nimbolide
1 isoflavones
1 α-Santalol/Sandalwood oil
1 Scoulerine
1 SonoDynamic Therapy UltraSound
1 Shikonin
1 Aflavin-3,3′-digallate
1 Ursolic acid
1 Vitamin K2

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

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:43  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

Casp7 Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress(tgid=1) ⓘ

Mitochondria & Bioenergetics(tgid=3) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Kinase & Signal Transduction(tgid=6) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Protein Folding & ER Stress(tgid=8) ⓘ

Autophagy & Lysosomes(tgid=9) ⓘ

DNA Damage & Repair(tgid=10) ⓘ

Cell Cycle & Senescence(tgid=11) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Cellular Microenvironment(tgid=17) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

Pathway results for Effect on Normal Cells:

NA, unassigned(tgid=0) ⓘ

Redox & Oxidative Stress(tgid=1) ⓘ

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cell Death(tgid=5) ⓘ

Transcription & Epigenetics(tgid=7) ⓘ

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

Migration(tgid=13) ⓘ

Angiogenesis & Vasculature(tgid=14) ⓘ

Barriers & Transport(tgid=15) ⓘ

Immune & Inflammatory Signaling(tgid=16) ⓘ

Hormonal & Nuclear Receptors(tgid=20) ⓘ

Drug Metabolism & Resistance(tgid=21) ⓘ

Clinical Biomarkers(tgid=22) ⓘ

Functional Outcomes(tgid=23) ⓘ

Infection & Microbiome(tgid=24) ⓘ

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