Wnt/(β-catenin) Cancer Research Results
Wnt/(β-catenin), Wnt/(β-catenin): Click to Expand ⟱
| Source: HalifaxProj (inhibit)
TCGA |
| Type: |
The Wnt signaling pathway is activated when Wnt proteins bind to Frizzled receptors on the cell surface, leading to the stabilization and accumulation of β-catenin in the cytoplasm and its subsequent translocation to the nucleus.
In the nucleus, β-catenin interacts with transcription factors to activate target genes that promote cell growth and survival.
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Scientific Papers found: Click to Expand⟱
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in-vivo, |
CRC, |
HCT116 |
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in-vitro, |
CRC, |
SW480 |
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ChemoSen↑, combined treatment
Casp9↑,
Ferroptosis↑, activation of ferroptosis and suppression of β-catenin/Wnt-signaling pathways were the key mediators for the anti-cancer and chemosensitizing effects of andrographis.
Wnt/(β-catenin)↓,
FTL↑,
TP53↑,
ACSL5↑,
GCLC↑,
GCLM↑,
SAT1↑,
STEAP3↑,
ACSL5↑,
*BioAv↓, Apigenin is not easily absorbed orally because of its low water solubility, which is only 2.16 g/mL
*Half-Life∅, Apigenin is slowly absorbed and eliminated from the body, as evidenced by its half‐life of 91.8 h in the blood
selectivity↑, selective anticancer effects and effective cell cytotoxic activity while exhibiting negligible toxicity to ordinary cells
*toxicity↓, intentional consumption in higher doses, as the toxicity hazard is low
Wnt/(β-catenin)↓, inhibiting the Wnt/β‐catenin
P53↑,
P21↑,
PI3K↓,
Akt↓,
mTOR↓,
TumCCA↑, G2/M
TumCI↓,
TumCMig↓,
STAT3↓, apigenin can activate p53, which improves catalase and inhibits STAT3,
PKM2↓,
EMT↓, reversing increases in epithelial–mesenchymal transition (EMT)
cl‑PARP↑, apigenin increases the cleavage of poly‐(ADP‐ribose) polymerase (PARP) and rapidly enhances caspase‐3 activity,
Casp3↑,
Bax:Bcl2↑,
VEGF↓, apigenin suppresses VEGF transcription
Hif1a↓, decrease in hypoxia‐inducible factor 1‐alpha (HIF‐1α
Dose∅, effectiveness of apigenin (200 and 300 mg/kg) in treating CC was evaluated by establishing xenografts on Balb/c nude mice.
GLUT1↓, Apigenin has been found to inhibit GLUT1 activity and glucose uptake in human pancreatic cancer cells
GlucoseCon↓,
TNF-α↓, Apigenin downregulates the TNFα
IL6↓,
IL1α↓,
P53↑,
Bcl-xL↓,
Bcl-2↓,
BAX↑,
Hif1a↓, Apigenin inhibited HIF-1alpha and vascular endothelial growth factor expression
VEGF↓,
TumCCA↑, Apigenin exposure induces G2/M phase cell cycle arrest, DNA damage, apoptosis and p53 accumulation
DNAdam↑,
Apoptosis↑,
CycB/CCNB1↓,
cycA1/CCNA1↓,
CDK1↓,
PI3K↓,
Akt↓,
mTOR↓,
IKKα↓, , decreases IKKα kinase activity,
ERK↓,
p‑Akt↓,
p‑P70S6K↓,
p‑S6↓,
p‑ERK↓, decreased
the expression of phosphorylated (p)-ERK1/2 proteins, p-AKT and p-mTOR
p‑P90RSK↑,
STAT3↓,
MMP2↓, Apigenin down-regulated Signal transducer and activator of transcription 3target genes MMP-2, MMP-9 and vascular endothelial growth factor
MMP9↓,
TumCP↓, Apigenin significantly suppressed colorectal cancer cell proliferation, migration, invasion and organoid growth through inhibiting the Wnt/β-catenin signaling
TumCMig↓,
TumCI↓,
Wnt/(β-catenin)↓,
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in-vitro, |
CRC, |
HCT116 |
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in-vitro, |
CRC, |
SW480 |
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Wnt/(β-catenin)↓,
β-catenin/ZEB1↓,
TumAuto↑,
Akt↓,
mTOR↓,
tumCV↓,
TumCCA↑, cell cycle arrest at G2/M phase
TumAuto↑, data suggested the involvement of autophagy in apigenin-induced β-catenin down-regulation during Wnt signaling
p‑Akt↓,
p‑p70S6↓,
p‑4E-BP1↓,
PI3K/Akt↓,
NF-kB↓,
CK2↓,
FOXO↓,
MAPK↝, modulation of MAPKs by apigenin contributed to apigenin-induced cell cycle arrest at G0/G1 phase
ERK↓, p-ERK1/2,
p‑JAK↓, phosphorylation
Wnt/(β-catenin)↓,
ROS↑, accumulation of reactive oxygen species (ROS) production, leading to induction of DNA damage
CDC25↓,
p‑STAT↓,
DNAdam↑,
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in-vitro, |
CRC, |
SW480 |
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in-vitro, |
CRC, |
HTC15 |
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Wnt/(β-catenin)↓, Apigenin inhibits β‑catenin/TCF/LEF signal activation.
TCF↓,
LEF1↓, LEF
TumCP↓, Apigenin inhibits CRC cell line proliferation
TumCMig↓, Apigenin inhibits migration and invasion of SW480 cells and growth of intestinal organoids.
TumCI↓,
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vitro+vivo, |
NSCLC, |
A549 |
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vitro+vivo, |
NSCLC, |
H1299 |
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TumCCA↑, arresting cell cycle in G1
phase.
CSCs↓,
TumCI↓,
TumCMig↓,
TumCG↓,
Wnt/(β-catenin)↓, main pathway
Nanog↓,
SOX2↓,
OCT4↓, oct3/4
N-cadherin↓,
Vim↓,
E-cadherin↑,
IL6↓,
IL1↓, IL-1β
TNF-α↓,
TGF-β↓, TGF-β1
NF-kB↓,
MIP2↓,
PGE2↓,
NO↓,
Hif1a↓,
KDR/FLK-1↓,
VEGF↓,
MMP2↓,
TIMP2↑,
ITGB1↑,
NCAM↑,
p‑ATM↑,
p‑ATR↑,
p‑CHK1↑,
p‑Chk2↑,
Wnt/(β-catenin)↓,
PI3K↓,
Akt↓,
ERK↓, ERK1/2
cMyc↓,
mTOR↓,
survivin↓,
cMET↓,
EGFR↓,
cycD1/CCND1↓,
cycE1↓,
CDK4/6↓,
p16↑,
p27↑,
Apoptosis↑,
TumAuto↑,
Ferroptosis↑,
oncosis↑,
TumCCA↑, G0/G1 into M phase, G0/G1 into S phase, G1 and G2/M
ROS↑, ovarian cancer cell line model, artesunate induced oxidative stress, DNA double-strand breaks (DSBs) and downregulation of RAD51 foci
DNAdam↑,
RAD51↓,
HR↓,
*AntiCan↑, capsaicin possesses anti-cancer, anti-inflammatory, and antioxidant properties and is used as a topical analgesic
*Inflam↓,
*antiOx↑,
*TRPV1↑, Studies demonstrate that capsaicin directly activates TRPV1 by binding to intracellular sites within the channel protein
*AMPK↑, Moreover, capsaicin and TRPV1 can activate the AMPK pathway [82, 83]
*SIRT1↑, elevating SIRT1 levels
*NADPH↓, suppressing NADPH oxidase and reducing reactive oxygen species
*ROS↓,
*MAPK↓, inhibiting MAPK pathways
*eNOS↑, activating eNOS
*Wnt/(β-catenin)↓, inhibiting the Wnt/β-catenin signaling pathway
RenoP↑, Furthermore, TRPV1 activation decreases renal perfusion pressure while increasing glomerular filtration rate and the excretion of sodium/water, thereby modulating renal hemodynamics and excretory functions
*Inflam↓, Monoterpenes like thymol and carvacrol are recognized for their anti‐inflammatory and anticancer properties,
AntiCan↑,
PI3K↓, Thymol derivatives, such as 1,2,3‐triazoles and carvacrol, effectively target breast cancer (BC) through PI3K/AKT/mTOR and NOTCH pathways and inhibit PIK3CA expression.
Akt↓,
mTOR↓,
NOTCH↓,
PIK3CA↓,
EGFR↓, thymol exhibits anti‐EGFR activity, while carvacrol modulates the HIF‐1α/VEGF pathway, making them potential candidates for colorectal cancer (CRC) management.
Hif1a↓,
VEGF↓,
ChemoSen↑, Their synergistic potential with chemotherapy, radiotherapy, and other bioactive compounds strengthens their therapeutic promise.
RadioS↑,
eff↝, challenges such as stability, bioavailability, and the need for clinical trials hinder their clinical application.
*cardioP↑, cardioprotective (Joshi et al. 2023), neuroprotective (Forqani et al. 2023) and hepato‐nephroprotective
*neuroP↑,
*hepatoP↑,
Apoptosis↑, Induction of Apoptosis
MMP↓, The apoptosis was due to ROS production, variations in the mitochondrial membrane, caspase‐3 activation, and DNA damage
Casp3↑,
ROS↑,
DNAdam↑,
eff↑, Thymol derivative, known as compound 10 (IC50 6.17 μM) exhibited 3.2‐fold more inhibition than 5‐fluorouracil (IC50 20.09 μM) against MCF‐7
BAX↑, Carvacrol (25, 50, 75, and 90 μM) enhanced the expression of Bax, Bad, Fas‐L, and cytochrome c, activated caspase‐9/3 and caspase‐8, induced cell cycle at G0/G1
BAD↑,
FasL↑,
Cyt‑c↑,
Casp9↑,
Casp8↑,
TumCCA↑,
P21↑, improved the expression of proteins (p21, cyclin D1, CDK4), and downregulated the SMO and GLI1 proteins expression in CC
Smo↓,
Gli1↓,
JNK↑, Moreover, thymol activated JNK and p38 MAPK while impeding the ERK pathway
ERK↓,
MAPK↓, Besides thymol, carvacrol has also been reported to inhibit MAPK or ERK pathways in previous studies.
TRPM7↓, inhibited TRPM7 expression in liver fibrotic C57BL/6J mice
Wnt/(β-catenin)↓, hymol inhibited HCT116 and LoVo cell line invasion via downregulating the Wnt/β‐catenin pathway and reducing c‐Myc and Cyclin D1 expression
BioAv↝, thymol and carvacrol are volatile, and their stability is influenced by these factors (temperature, light, oxygen, and pH)
BioAv↑, Ultrasonication is an effective technique to enhance the stability of thymol and other bioactive compounds. 400 watts of power elevated the performance of NC‐CH formulations, and NC‐CH‐400 displayed increased solubility.
Apoptosis↑,
TumCP↓,
TumCMig↓,
TumMeta↓,
EMT↓,
E-cadherin↑,
N-cadherin↓,
Snail↓,
Vim↓,
Hif1a↓,
Wnt/(β-catenin)↓,
AXIN1↑,
TumVol↓, orthotopic xenograft tumors
TumW↓,
TumCP↓, Celecoxib mainly regulates the proliferation, migration, and invasion of tumor cells by inhibiting the cyclooxygenases-2/prostaglandin E2 signal axis
TumCMig↓,
TumCI↓,
COX2↓,
p‑NF-kB↓, thereby inhibiting the phosphorylation of nuclear factor-κ-gene binding, Akt, signal transducer and activator of transcription and the expression of matrix metalloproteinase 2 and matrix metalloproteinase 9.
Akt↓,
MMP2↓,
MMP9↓,
Apoptosis↑, celecoxib could promote the apoptosis of tumor cells by enhancing mitochondrial oxidation, activating mitochondrial apoptosis process, promoting endoplasmic reticulum stress process, and autophagy.
mitResp↑,
ER Stress↑,
TumAuto↑,
ChemoSen↑, Celecoxib can also reduce the occurrence of drug resistance by increasing the sensitivity of cancer cells to chemotherapy drugs.
Inflam↓, NSAIDs achieve anti-inflammatory effects by inhibiting the activity of the inflammatory factor COX-2 and the synthesis of PGE2.
PGE2↓,
chemoPv↑, Numerous studies have confirmed that NSAIDs also have chemopreventive effects on tumors.
toxicity↓, Compared with other NSAIDs, celecoxib shows lower toxicity side effects (such as the most common gastrointestinal bleeding and gastric ulcer).[
Risk↓, Early studies have shown that celecoxib can effectively reduce the incidence of colorectal cancer, especially inhibiting the development of familial adenomatous polyposis to colorectal cancer.
PI3K↓, celecoxib can promote cancer cell apoptosis by inhibiting the signal pathway of 3-phosphoinositide-dependent kinase-1 and downstream protein kinase B (Akt) in human colon cancer cells.
RadioS↑, celecoxib enhances the sensitivity of cancer cells to radiation therapy
TumCMig↓, inhibits cancer cell migration and invasion by inhibiting the activity of C-Jun amino-terminal kinase and downregulating the expression of specific protein 1.
TumCI↓,
cJun↓,
Sp1/3/4↓,
ROS↑, Celecoxib targets mitochondria and promotes the release of ROS by significantly increased oxidative stress.
MMP↓, lead to the decrease of cell consumption and mitochondrial transmembrane potential (△ ψ m), increasing mitochondrial membrane permeability to promote the release of ROS
MPT↑,
Ca+2↑, promote Ca2+ influx, produce a higher pro-oxidation state, increase the accumulation of ROS in cancer cell mitochondria,
Glycolysis↓, inhibits the glycolysis process, ATP synthesis is significantly reduced, leading to cancer cell death.[
ATP↓,
CSCs↓, In addition to cancer cells, celecoxib can also inhibit CSCs.
Wnt/(β-catenin)↓, celecoxib can inhibit the transduction of Wnt/β-catenin signaling pathway
EMT↓, celecoxib can inhibit the process of EMT
toxicity↝, ong-term use increases the risk of hypertension among participants who already have cardiovascular risk factors.[
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in-vitro, |
Lung, |
A549 |
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in-vitro, |
Lung, |
H1299 |
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HH↓,
Wnt/(β-catenin)↓, curcumin suppressed the activation of both Wnt/β-catenin and Sonic Hedgehog pathways. T
Shh↓,
Smo↓,
Gli1↝,
GLI2↝,
CSCs↓, Curcumin Suppresses Lung Cancer Stem Cells via Inhibiting Wnt/β-catenin and Sonic Hedgehog Pathways
CD133↓, reduced number of CD133-positive cells, decreased expression levels of lung CSC markers,
CSCsMark↓,
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in-vitro, |
Ovarian, |
SKOV3 |
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Wnt/(β-catenin)↓,
EMT↓,
DNMT3A↓,
cycD1/CCND1↓,
cMyc↓,
Fibronectin↓,
Vim↓,
E-cadherin↑,
SFRP5↑,
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in-vitro, |
BC, |
4T1 |
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in-vitro, |
BC, |
MCF-7 |
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in-vivo, |
BC, |
NA |
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TumCG↓,
TumCCA↑, induced G1 cell cycle arrest
β-catenin/ZEB1↓,
TCF↓,
LEF1↓,
cMyc↓,
cycD1/CCND1↓,
Wnt/(β-catenin)↓,
TumMeta↓,
*BioAv↓, Within the gastrointestinal tract, EA has restricted bioavailability, primarily due to its hydrophobic nature and very low water solubility.
antiOx↓, strong antioxidant properties [12,13], anti-inflammatory effects
Inflam↓,
TumCP↓, numerous studies indicate that EA possesses properties that can inhibit cell proliferation
TumCCA↑, achieved this by causing cell cycle arrest at the G1 phase
cycD1/CCND1↓, reduction of cyclin D1 and E levels, as well as to the upregulation of p53 and p21 proteins
cycE/CCNE↓,
P53↑,
P21↑,
COX2↓, notable reduction in the protein expression of COX-2 and NF-κB as a result of this treatment
NF-kB↓,
Akt↑, suppressing Akt and Notch signaling pathways
NOTCH↓,
CDK2↓,
CDK6↓,
JAK↓, suppression of the JAK/STAT3 pathway
STAT3↓,
EGFR↓, decreased expression of epidermal growth factor receptor (EGFR)
p‑ERK↓, downregulated the expression of phosphorylated ERK1/2, AKT, and STAT3
p‑Akt↓,
p‑STAT3↓,
TGF-β↓, downregulation of the TGF-β/Smad3
SMAD3↓,
CDK6↓, EA demonstrated the capacity to bind to CDK6 and effectively inhibit its activity
Wnt/(β-catenin)↓, ability of EA to inhibit phosphorylation of EGFR
Myc↓, Myc, cyclin D1, and survivin, exhibited decreased levels
survivin↓,
CDK8↓, diminished CDK8 level
PKCδ↓, EA has demonstrated a notable downregulatory impact on the expression of classical isoenzymes of the PKC family (PKCα, PKCβ, and PKCγ).
tumCV↓, EA decreased cell viability
RadioS↑, further intensified when EA was combined with gamma irradiation.
eff↑, EA additionally potentiated the impact of quercetin in promoting the phosphorylation of p53 at Ser 15 and increasing p21 protein levels in the human leukemia cell line (MOLT-4)
MDM2↓, finding points to the ability of reduced MDM2 levels
XIAP↓, downregulation of X-linked inhibitor of apoptosis protein (XIAP).
p‑RB1↓, EA exerted a decrease in phosphorylation of pRB
PTEN↑, EA enhances the protein phosphatase activity of PTEN in melanoma cells (B16F10)
p‑FAK↓, reduced phosphorylation of focal adhesion kinase (FAK)
Bax:Bcl2↑, EA significantly increases the Bax/Bcl-2 rati
Bcl-xL↓, downregulates Bcl-xL and Mcl-1
Mcl-1↓,
PUMA↑, EA also increases the expression of Bcl-2 inhibitory proapoptotic proteins PUMA and Noxa in prostate cancer cells
NOXA↑,
MMP↓, addition to the reduction in MMP, the release of cytochrome c into the cytosol occurs in pancreatic cancer cells
Cyt‑c↑,
ROS↑, induction of ROS production
Ca+2↝, changes in intracellular calcium concentration, leading to increased levels of EndoG, Smac/DIABLO, AIF, cytochrome c, and APAF1 in the cytosol
Endoglin↑,
Diablo↑,
AIF↑,
iNOS↓, decreased expression of Bcl-2, NF-кB, and iNOS were observed after exposure to EA at concentrations of 15 and 30 µg/mL
Casp9↑, increase in caspase 9 activity in EA-treated pancreatic cancer cells PANC-1
Casp3↑, EA-induced caspase 3 activation and PARP cleavage in a dose-dependent manner (10–100 µmol/L)
cl‑PARP↑,
RadioS↑, EA sensitizes and reduces the resistance of breast cancer MCF-7 cells to apoptosis induced by γ-radiation
Hif1a↓, EA reduced the expression of HIF-1α
HO-1↓, EA significantly reduced the levels of two isoforms of this enzyme, HO-1, and HO-2, and increased the levels of sEH (Soluble epoxide hydrolase) in LnCap
HO-2↓,
SIRT1↓, EA-induced apoptosis was associated with reduced expression of HuR and Sirt1
selectivity↑, A significant advantage of EA as a potential chemopreventive, anti-tumor, or adjuvant therapeutic agent in cancer treatment is its relative selectivity
Dose∅, EA significantly reduced the viability of cancer cells at a concentration of 10 µmol/L, while in healthy cells, this effect was observed only at a concentration of 200 µmol/L
NHE1↓, EA had the capacity to regulate cytosolic pH by downregulating the expression of the Na+/H+ exchanger (NHE1)
Glycolysis↓, led to intracellular acidification with subsequent impairment of glycolysis
GlucoseCon↓, associated with a decrease in the cellular uptake of glucose
lactateProd↓, notable reduction in lactate levels in supernatant
PDK1?, inhibit pyruvate dehydrogenase kinase (PDK) -bind and inhibit PDK3
PDK1?,
ECAR↝, EA has been shown to influence extracellular acidosis
COX1↓, downregulation of cancer-related genes, including COX1, COX2, snail, twist1, and c-Myc.
Snail↓,
Twist↓,
cMyc↓,
Telomerase↓, EA, might dose-dependently inhibit telomerase activity
angioG↓, EA may inhibit angiogenesis
MMP2↓, EA demonstrated a notable reduction in the secretion of matrix metalloproteinase (MMP)-2 and MMP-9.
MMP9↓,
VEGF↓, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
Dose↝, At lower concentrations (10 and 20 μM), EA led to a substantial increase in VEGF levels. However, at higher doses (40 and 100 μM), a notable reduction in VEGF
PD-L1↓, EA downregulated the expression of the immune checkpoint PD-L1 in tumor cells
eff↑, EA might potentially enhance the efficacy of anti-PD-L1 treatment
SIRT6↑, EA exhibited statistically significant upregulation of sirtuin 6 at the protein level in Caco2 cells
DNAdam↓, increase in DNA damage
ROS↑, pomegranate ET inhibit pro-inflammatory pathways including, but not limited to, the NF-κB pathway, whose activation leads to immune reactions, inflammation, and the transcription of genes involved in cell survival, such as Bclx and inhibitors of apop
angioG↓, ET to inhibit angiogenesis
ChemoSen↑, ET could also be utilized to increase the sensitivity of tumor cells to standard chemotherapeutic drugs
BAX↑, induction of pro-apoptotic mediators (Bax and Bak), downregulation of Bcl-2 and Bcl-XL, and reduced expression of cyclin-dependent kinases 2, 4, 6, and cyclins D1, D2, and E
Bak↑,
Bcl-2↓,
Bcl-xL↓,
CDK2↓,
CDK4↓,
CDK6↓,
cycD1/CCND1↓,
cycE1↓,
TumCG↓, reduced LNCaP prostate cancer xenograft size, tumor vessel density, VEGF peptide levels and HIF-α expression after four weeks of treatment in severe combined immunodeficient mice
VEGF↓,
Hif1a↓,
eff↑, Oenothein B, a macrocyclic ET, and quercetin-3-O-glucuronide from Epilobium sp. herbs—used in traditional medicine to treat benign prostatic hyperplasia and prostatic adenoma—have been proven to strongly inhibit the proliferation of human prostate ca
COX2↓, pomegranate ET (i.e., punicalagin and ellagic acid) have been shown to suppress cyclooxygenase-2 (COX-2) protein expression in human colon cancer (HT-29) cells
TumCCA↑, pomegranate ET and their metabolites, i.e., urolithins A and C, inhibit HT-29 cells proliferation via G0/G1 and G2/M arrest
selectivity↑, interestingly, normal human breast epithelial cells (MCF-10A) were far less sensitive to the inhibitory effect of polyphenol-rich fractions.
Wnt/(β-catenin)↓, suppression of Wnt/β-catenin
*toxicity∅, LD50 of a standardized pomegranate fruit extract containing 30% punicalagin in Wistar rats was >5 g/kg b.w.,
TumCP↓,
TumCCA↑, G0/G1 phase arrest
Wnt/(β-catenin)↓,
EMT↓,
ERK↓, ERK1/2
PI3K/Akt↓,
Wnt/(β-catenin)↓,
STAT3↓,
NF-kB↓,
ChemoSen↑, cisplatin or paclitaxel, in the presence of garcinol can lead to a significant increase in the treatment outcome
COX2↓,
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
VEGF↓,
TGF-β↓,
HATs↓,
E-cadherin↑,
Vim↓,
Zeb1↓,
ZEB2↓,
Let-7↑,
MMP9↓,
TumCCA↑, cycle arrest at G0/G1 phase
ROS↑,
MMP↓,
IL6↓,
NOTCH1↓,
Wnt/(β-catenin)↓,
ALDH1A1↓,
LRP6↓,
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vitro+vivo, |
Ovarian, |
SKOV3 |
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Wnt/(β-catenin)↓,
mTOR↓,
STAT3↓,
NF-kB↓,
NOTCH↓,
TumCG↓,
Apoptosis↑,
MEK↓, inactivating MEK1/2-ERK1/2
ERK↓,
mitResp↓,
Glycolysis↓, aerobic glycolysis
ROS↑, abolishment of the excess ROS production with NAC (10 mM) abrogated the Niclosamide-induced cell apoptosis under glucose deprivation
JNK↑,
CycB/CCNB1↓, quercetin has a role in the reduction of cyclin B1 and CDK1 levels,
CDK1↓,
EMT↓, quercetin suppresses epithelial to mesenchymal transition (EMT) and cell proliferation through modulation of Sonic Hedgehog signaling pathway
PI3K↓, Inhibitory effects of quercetin on other pathways such as PI3K, MAPK and WNT pathways have also been validated in cervical cancer
MAPK↓,
Wnt/(β-catenin)↓, wnt
PSA↓,
VEGF↓,
PARP↑,
Casp3↑,
Casp9↑,
DR5↑,
ROS⇅,
Shh↓,
P53↑, figure 1
P21↑, quercetin regulates p21 expression
EGFR↓,
TumCCA↑, quercetin has cell-specific anti-proliferative impacts via stimulation of cell cycle arrest at the G1 stage.
ROS↑, quercetin has been shown to suppress carcinogenesis through various mechanisms including affecting cell proliferation, production of reactive oxygen species and expression of miR-21
miR-21↓,
TumCP↓,
selectivity↑, In breast cancer cells, quercetin inhibits cell proliferation without exerting any cytotoxic impact on normal breast epithelium
PDGF↓, figure 1
EGF↓,
TNF-α↓,
VEGFR2↓,
mTOR↓,
cMyc↓,
MMPs↓,
GRP78/BiP↑,
CHOP↑,
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in-vitro, |
Colon, |
CX-1 |
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in-vitro, |
Colon, |
SW480 |
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in-vitro, |
Colon, |
HT-29 |
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in-vitro, |
Colon, |
HCT116 |
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cycD1/CCND1↓, Cyclin D(1) and the survivin gene were downregulated markedly by quercetin in a dose-dependent manner
survivin↓,
Wnt/(β-catenin)↓, Quercetin downregulated transcriptional activity of beta-catenin/Tcf in SW480 cells transiently transfected with the TCF-4 reporter gene.
tumCV↓, Quercetin reduced cell viability in a dose- and time-dependent manner in SW480 and clone 26 cells
TumCCA↑, The percentages of SW480 cells and clone 26 cells at G(2)/M phase were increased significantly after treatment with 40 approximately 80 micromol/L quercetin for 48 hours.
Apoptosis↑, Quercetin induced the apoptosis of SW480 cells in a dose-dependent manner at the concentration of 20, 40, 60, anf 80 micromol/L.
tumCV↓,
Apoptosis↑,
PI3k/Akt/mTOR↓, QUE induces cell death by inhibiting PI3K/Akt/mTOR and STAT3 pathways in PEL cells
Wnt/(β-catenin)↓, reducing β-catenin
MAPK↝,
ERK↝, ERK1/2
TumCCA↑, cell cycle arrest at the G1 phase
H2O2↑,
ROS↑,
TumAuto↑,
MMPs↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
P53↑,
Casp3↑,
Hif1a↓, by inactivating the Akt-mTOR pathway [64,74] and HIF-1α
cFLIP↓,
IL6↓, QUE decreased the release of interleukin-6 (IL-6) and IL-10
IL10↓,
lactateProd↓,
Glycolysis↓, It is suggested that QUE alters glucose metabolism by inhibiting monocarboxylate transporter (MCT) activity
PKM2↓,
GLUT1↓,
COX2↓,
VEGF↓,
OCR↓,
ECAR↓,
STAT3↓,
MMP2↓, Consistently, QUE was able to reduce the protein levels of MMP-2, MMP-9, VEGF and mTOR, and p-Akt in breast cancer cell lines
MMP9:TIMP1↓,
mTOR↓,
| - |
in-vitro, |
CRC, |
LoVo |
|
|
|
- |
in-vitro, |
CRC, |
HCT116 |
|
|
|
MALAT1↓,
Wnt/(β-catenin)↓,
TumCI↓,
TumMeta↓,
PI3K↓,
Akt↓,
NF-kB↓,
Wnt/(β-catenin)↓,
MAPK↓,
TumCP↓,
TumCCA↑, G0/G1 cell cycle arrest
Apoptosis↑, In T24 and UM-UC-3 human bladder cancer cells, silibinin treatment at a concentration of 10 μM significantly inhibited proliferation, migration, invasion, and induced apoptosis.
p‑EGFR↓,
JAK2↓,
STAT5↓,
cycD1/CCND1↓,
hTERT/TERT↓,
AP-1↓,
MMP9↓,
miR-21↓,
miR-155↓,
Casp9↑,
BID↑,
ERK↓, ERK1/2
Akt2↓,
DNMT1↓,
P53↑,
survivin↓,
Casp3↑,
ROS↑, cytotoxicity of silibinin in Hep-2 cells was associated with the accumulation of intracellular reactive oxygen species (ROS), which could be mitigated by the ROS scavenger NAC.
TumCP↓, thymol treatment in vitro inhibited cell proliferation and induced apoptosis and cell cycle arrest in CRC.
Apoptosis↑,
TumVol↓, in vivo treatment with 75 and 150 mg/kg thymol led to a significant decrease in tumor volume.
Bax:Bcl2↑, activation of the BAX/Bcl-2 signaling pathway
EMT↓, thymol suppressed CRC cell epithelial–mesenchymal transition (EMT), invasion, and metastasis via inhibiting the activation of the Wnt/β-catenin pathway, both in vitro and in vivo.
TumCI↓,
TumMeta↓,
Wnt/(β-catenin)↓,
Showing Research Papers: 1 to 27 of 27
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 27
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
antiOx↓, 1, Ferroptosis↑, 2, GCLC↑, 1, GCLM↑, 1, H2O2↑, 1, HO-1↓, 1, HO-2↓, 1, ROS↑, 11, ROS⇅, 1,
Metal & Cofactor Biology ⓘ
FTL↑, 1, STEAP3↑, 1,
Mitochondria & Bioenergetics ⓘ
AIF↑, 1, ATP↓, 1, CDC25↓, 1, EGF↓, 1, MEK↓, 1, mitResp↓, 1, mitResp↑, 1, MMP↓, 4, MPT↑, 1, OCR↓, 1, XIAP↓, 1,
Core Metabolism/Glycolysis ⓘ
ACSL5↑, 2, cMyc↓, 5, ECAR↓, 1, ECAR↝, 1, GlucoseCon↓, 2, Glycolysis↓, 4, lactateProd↓, 2, PDK1?, 2, PI3K/Akt↓, 2, PI3k/Akt/mTOR↓, 1, PIK3CA↓, 1, PKM2↓, 2, p‑S6↓, 1, SAT1↑, 1, SIRT1↓, 1,
Cell Death ⓘ
Akt↓, 7, Akt↑, 1, p‑Akt↓, 3, Apoptosis↑, 10, BAD↑, 1, Bak↑, 1, BAX↑, 4, Bax:Bcl2↑, 3, Bcl-2↓, 3, Bcl-xL↓, 3, BID↑, 1, Casp3↑, 7, Casp8↑, 1, Casp9↑, 6, cFLIP↓, 1, p‑Chk2↑, 1, CK2↓, 1, Cyt‑c↑, 2, Diablo↑, 1, DR5↑, 1, FasL↑, 1, Ferroptosis↑, 2, hTERT/TERT↓, 1, iNOS↓, 1, JNK↑, 2, MAPK↓, 3, MAPK↝, 2, Mcl-1↓, 1, MDM2↓, 1, Myc↓, 1, NOXA↑, 1, oncosis↑, 1, p27↑, 1, PUMA↑, 1, survivin↓, 4, Telomerase↓, 1,
Kinase & Signal Transduction ⓘ
p‑p70S6↓, 1, Sp1/3/4↓, 1,
Transcription & Epigenetics ⓘ
cJun↓, 1, HATs↓, 1, miR-21↓, 2, tumCV↓, 4,
Protein Folding & ER Stress ⓘ
CHOP↑, 1, ER Stress↑, 1, GRP78/BiP↑, 1,
Autophagy & Lysosomes ⓘ
TumAuto↑, 5,
DNA Damage & Repair ⓘ
p‑ATM↑, 1, p‑ATR↑, 1, p‑CHK1↑, 1, DNAdam↓, 1, DNAdam↑, 4, DNMT1↓, 1, DNMT3A↓, 1, HR↓, 1, p16↑, 1, P53↑, 6, PARP↑, 1, cl‑PARP↑, 2, RAD51↓, 1, SIRT6↑, 1, TP53↑, 1,
Cell Cycle & Senescence ⓘ
CDK1↓, 2, CDK2↓, 2, CDK4↓, 1, cycA1/CCNA1↓, 1, CycB/CCNB1↓, 2, cycD1/CCND1↓, 7, cycE/CCNE↓, 1, cycE1↓, 2, P21↑, 4, p‑RB1↓, 1, TumCCA↑, 15,
Proliferation, Differentiation & Cell State ⓘ
p‑4E-BP1↓, 1, ALDH1A1↓, 1, AXIN1↑, 1, CD133↓, 1, CDK8↓, 1, cMET↓, 1, CSCs↓, 3, CSCsMark↓, 1, EMT↓, 7, ERK↓, 7, ERK↝, 1, p‑ERK↓, 2, FOXO↓, 1, Gli1↓, 1, Gli1↝, 1, HH↓, 1, Let-7↑, 1, LRP6↓, 1, mTOR↓, 8, Nanog↓, 1, NOTCH↓, 3, NOTCH1↓, 1, OCT4↓, 1, p‑P70S6K↓, 1, p‑P90RSK↑, 1, PI3K↓, 7, PTEN↑, 1, SFRP5↑, 1, Shh↓, 2, Smo↓, 2, SOX2↓, 1, p‑STAT↓, 1, STAT3↓, 6, p‑STAT3↓, 1, STAT5↓, 1, TCF↓, 2, TRPM7↓, 1, TumCG↓, 4, Wnt/(β-catenin)↓, 26,
Migration ⓘ
Akt2↓, 1, AP-1↓, 1, Ca+2↑, 1, Ca+2↝, 1, CDK4/6↓, 1, E-cadherin↑, 4, p‑FAK↓, 1, Fibronectin↓, 1, GLI2↝, 1, ITGB1↑, 1, LEF1↓, 2, MALAT1↓, 1, miR-155↓, 1, MMP2↓, 5, MMP9↓, 5, MMP9:TIMP1↓, 1, MMPs↓, 2, N-cadherin↓, 2, NCAM↑, 1, PDGF↓, 1, PKCδ↓, 1, SMAD3↓, 1, Snail↓, 2, TGF-β↓, 3, TIMP2↑, 1, TumCI↓, 8, TumCMig↓, 7, TumCP↓, 9, TumMeta↓, 4, Twist↓, 1, Vim↓, 4, Zeb1↓, 1, ZEB2↓, 1, β-catenin/ZEB1↓, 2,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 4, p‑EGFR↓, 1, Endoglin↑, 1, Hif1a↓, 8, KDR/FLK-1↓, 1, NO↓, 1, VEGF↓, 9, VEGFR2↓, 1,
Barriers & Transport ⓘ
GLUT1↓, 2, NHE1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX1↓, 1, COX2↓, 5, IKKα↓, 1, IL1↓, 1, IL10↓, 1, IL1α↓, 1, IL6↓, 4, Inflam↓, 2, JAK↓, 1, p‑JAK↓, 1, JAK2↓, 1, MIP2↓, 1, NF-kB↓, 6, p‑NF-kB↓, 1, PD-L1↓, 1, PGE2↓, 2, PSA↓, 1, TNF-α↓, 3,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 3,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, BioAv↝, 1, ChemoSen↑, 5, Dose↝, 1, Dose∅, 2, eff↑, 4, eff↝, 1, RadioS↑, 4, selectivity↑, 4,
Clinical Biomarkers ⓘ
EGFR↓, 4, p‑EGFR↓, 1, hTERT/TERT↓, 1, IL6↓, 4, Myc↓, 1, PD-L1↓, 1, PSA↓, 1, TP53↑, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, chemoPv↑, 1, RenoP↑, 1, Risk↓, 1, toxicity↓, 1, toxicity↝, 1, TumVol↓, 2, TumW↓, 1,
Total Targets: 237
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, ROS↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, NADPH↓, 1, SIRT1↑, 1,
Cell Death ⓘ
MAPK↓, 1, TRPV1↑, 1,
Proliferation, Differentiation & Cell State ⓘ
Wnt/(β-catenin)↓, 1,
Angiogenesis & Vasculature ⓘ
eNOS↑, 1,
Immune & Inflammatory Signaling ⓘ
Inflam↓, 2,
Drug Metabolism & Resistance ⓘ
BioAv↓, 2, Half-Life∅, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cardioP↑, 1, hepatoP↑, 1, neuroP↑, 1, toxicity↓, 1, toxicity∅, 1,
Total Targets: 18
Scientific Paper Hit Count for: Wnt/(β-catenin), Wnt/(β-catenin)
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#:338 State#:% Dir#:1
wNotes=on sortOrder:rid,rpid
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