YAP/TEAD Cancer Research Results

YAP/TEAD, YAP/TEAD activity: Click to Expand ⟱
Source: HalifaxProj (inhibit)
Type:
YAP (Yes-associated protein) and TEAD (TEA domain transcription factors) are key components of the Hippo signaling pathway, which plays a crucial role in regulating cell growth, proliferation, and apoptosis.
Activation of YAP: In normal conditions, the Hippo pathway inhibits YAP activity, preventing excessive cell growth. However, when the Hippo pathway is inactivated (due to mutations or other factors), YAP becomes activated. This leads to increased cell proliferation and survival, contributing to tumorigenesis.
TEAD as a Transcription Factor: YAP interacts with TEAD proteins to drive the expression of target genes that promote cell growth and inhibit apoptosis. This YAP/TEAD complex is often found to be overactive in several types of cancer, including liver, breast, and lung cancers.
Scientific Papers found: Click to Expand⟱
5380- ART/DHA,    Artemisinin and Its Derivatives as Potential Anticancer Agents
- Review, Var, NA
TumCG↓, Artemisinin (1, Figure 2) could suppress cell growth [16], reduce angiogenesis-related factors [17], and induce ferroptosis [18] in breast cancer cell lines
angioG↓,
Ferroptosis↑,
TumCP↑, Dihydroartemisinin (2, Figure 2) exhibited anticancer effects against breast cancer by suppressing cell proliferation [16], inhibiting angiogenesis [19], inducing autophagy [20] and pyroptosis [21], and targeting cancer stem cells (CSCs) [
TumAuto↑,
CSCs↑,
eff↑, Dihydroartemisinin is more potent than artemisinin, as the IC50 values at 24 h were lower on MCF-7 (129.1 μM versus 396.6 μM) and MDA-MB-231 (62.95 μM versus 336.63 μM)
YAP/TEAD↓, Additionally, dihydroartemisinin was proven to have the ability to reduce the expression of yes-associated protein 1 (YAP1), which has been commonly used as a prognostic marker in liver cancer.
TumCCA↑, induced G0/G1 cell cycle arrest and apoptosis by promoting oxygen species (ROS) accumulation.
ROS↑,
ChemoSen↑, The application of combination treatment using artemisinin and its derivatives with commonly used chemotherapy drugs, such as cisplatin, carboplatin, doxorubicin, temozolomide, etc., always exhibits significantly improved anticancer effects
N-cadherin↓, and inhibiting the proliferation, colony formation, and invasiveness of colon cancer cells by inhibiting NRP2, N-cadherin, and Vimentin expression
Vim↓,
MMP9↓, by decreasing the expression of HuR and matrix metalloproteinase (MMP)-9 proteins [24],
eff↑, Further investigations suggested that both dihydroartemisinin treatment and the loss of PRIM2 could lead to a decreased GSH level and induce cellular lipid ROS and mitochondrial MDA expression.
STAT3↓, Recently, artemisinin and its derivatives were reported to have potential as direct STAT3 inhibitors [98].
CD133↓, dihydroartemisinin treatment could significantly reduce the expression of CSC markers (CD133, CD44, Nanog, c-Myc, and OCT4) by downregulating Akt/mTOR pathway
CD44↓,
Nanog↓,
cMyc↓,
OCT4↓,
Akt↓,
mTOR↓,

5719- BF,    Bufalin inhibits the proliferation of lung cancer cells by suppressing Hippo-YAP pathway
- in-vitro, Lung, NA
TumCP↓, Bufalin inhibits the proliferation of lung cancer cells in vivo / in vitro by suppressing Hippo-YAP pathway.
Hippo↓,
YAP/TEAD↓,

1125- LT,    Luteolin suppresses epithelial-mesenchymal transition and migration of triple-negative breast cancer cells by inhibiting YAP/TAZ activity
- in-vitro, BC, NA
YAP/TEAD↓,
TAZ↓,
MSCmark↓,
EM↑,
TumCMig↓,

2914- LT,    Therapeutic Potential of Luteolin on Cancer
- Review, Var, NA
*antiOx↑, As an antioxidant, Luteolin and its glycosides can scavenge free radicals caused by oxidative damage and chelate metal ions
*IronCh↑,
*toxicity↓, The safety profile of Luteolin has been proven by its non-toxic side effects, as the oral median lethal dose (LD50) was found to be higher than 2500 and 5000 mg/kg in mice and rats, respectively, equal to approximately 219.8−793.7 mg/kg in humans
*BioAv↓, One major problem related to the use of flavonoids for therapeutic purposes is their low bioavailability.
*BioAv↑, Resveratrol, which functions as the inhibitor of UGT1A1 and UGT1A9, significantly improved the bioavailability of Luteolin by decreasing the major glucuronidation metabolite in rats
DNAdam↑, Luteolin’s anticancer properties, which involve DNA damage, regulation of redox, and protein kinases in inhibiting cancer cell proliferation
TumCP↓,
DR5↑, Luteolin was discovered to promote apoptosis of different cancer cells by increasing Death receptors, p53, JNK, Bax, Cleaved Caspase-3/-8-/-9, and PARP expressions
P53↑,
JNK↑,
BAX↑,
cl‑Casp3↑,
cl‑Casp8↑,
cl‑Casp9↑,
cl‑PARP↑,
survivin↓, downregulating proteins involved in cell cycle progression, including Survivin, Cyclin D1, Cyclin B, and CDC2, and upregulating p21
cycD1/CCND1↓,
CycB/CCNB1↓,
CDC2↓,
P21↑,
angioG↓, suppress angiogenesis in cancer cells by inhibiting the expression of some angiogenic factors, such as MMP-2, AEG-1, VEGF, and VEGFR2
MMP2↓,
AEG1↓,
VEGF↓,
VEGFR2↓,
MMP9↓, inhibit metastasis by inhibiting several proteins that function in metastasis, such as MMP-2/-9, CXCR4, PI3K/Akt, ERK1/2
CXCR4↓,
PI3K↓,
Akt↓,
ERK↓,
TumAuto↑, can promote the conversion of LC3B I to LC3B II and upregulate Beclin1 expression, thereby causing autophagy
LC3B-II↑,
EMT↓, Luteolin was identified to suppress the epithelial to mesenchymal transition by upregulating E-cadherin and downregulating N-cadherin and Wnt3 expressions.
E-cadherin↑,
N-cadherin↓,
Wnt↓,
ROS↑, DNA damage that is induced by reactive oxygen species (ROS),
NICD↓, Luteolin can block the Notch intracellular domain (NICD) that is created by the activation of the Not
p‑GSK‐3β↓, Luteolin can inhibit the phosphorylation of the GSK3β induced by Wnt, resulting in the prevention of GSK3β inhibition
iNOS↓, Luteolin in colon cancer and the complications associated with it, particularly the decreasing effect on the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2)
COX2↓,
NRF2↑, Luteolin has been identified to increase the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), which is a crucial transcription factor with anticarcinogenic properties related
Ca+2↑, caused loss of the mitochondrial membrane action potential, enhanced levels of mitochondrial calcium (Ca2+),
ChemoSen↑, Luteolin enhanced the effect of one of the most effective chemotherapy drugs, cisplatin, on CRC cells
ChemoSen↓, high dose of Luteolin application negatively affected the oxaliplatin-based chemotherapy in a p53-dependent manner [52]. They suggested that the flavonoids with Nrf2-activating ability might interfere with the chemotherapeutic efficacy of anticancer
IFN-γ↓, decreased the expression of interferon-gamma-(IFN-γ)
RadioS↑, suggested that Luteolin can act as a radiosensitizer, promoting apoptosis by inducing p38/ROS/caspase cascade
MDM2↓, Luteolin treatment was associated with increased p53 and p21 and decreased MDM4 expressions both in vitro and in vivo.
NOTCH1↓, Luteolin suppressed the growth of lung cancer cells, metastasis, and Notch-1 signaling pathway
AR↓, downregulating the androgen receptor (AR) expression
TIMP1↑, Luteolin inhibits the migration of U251MG and U87MG human glioblastoma cell lines by downregulating MMP-2 and MMP-9 and upregulating the tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2.
TIMP2↑,
ER Stress↑, Luteolin caused oxidative stress and ER stress in the Hep3B cells,
CDK2↓, Luteolin’s ability to decrease Akt, polo-like kinase 1 (PLK1), cyclin B1, cyclin A, CDC2, cyclin-dependent kinase 2 (CDK2) and Bcl-xL
Telomerase↓, Luteolin dose-dependently inhibited the telomerase levels and caused the phosphorylation of NF-κB and the target gene of NF-κB, c-Myc to suppress the human telomerase reverse transcriptase (hTERT)
p‑NF-kB↑,
p‑cMyc↑,
hTERT/TERT↓,
RAS↓, Luteolin was found to suppress the expressions of K-Ras, H-Ras, and N-Ras, which are the activators of PI3K
YAP/TEAD↓, Luteolin caused significant inhibition of yes-associated protein (YAP)/transcriptional co-activator with PDZ-binding motif (TAZ)
TAZ↓,
NF-kB↓, Luteolin was found to have a strong inhibitory effect on the NF-κB
NRF2↓, Luteolin-loaded nanoparticles resulted in a significant reduction in the Nrf2 levels compared to Luteolin alone.
HO-1↓, The expressions of the downstream genes of Nrf2, Ho1, and MDR1 were also reduced, where inhibition of Nrf2 expression significantly increased the cell death of breast cancer cells
MDR1↓,

1042- MEL,    Melatonin Downregulates PD-L1 Expression and Modulates Tumor Immunity in KRAS-Mutant Non-Small Cell Lung Cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H460 - in-vitro, Lung, LLC1
PD-L1↓, we found that lung cancer cells harboring the KRAS mutation exhibited a higher level of programmed death ligand 1 (PD-L1). However, treatment with melatonin substantially downregulated PD-L1
YAP/TEAD↓,
TAZ↓,
TumCG↓, mouse

5242- MFrot,    Rotating magnetic field downregulating type XI collagen to suppress triple-negative breast cancer metastasis by inactivating the ITGB1/FAK/YAP signaling pathway
- in-vitro, BC, NA
TumCI↓, RMF can significantly inhibit the invasion and metastasis of TNBC cells.
COL11A1↓, Notably, COL11A1 was reduced following exposure to RMF.
TumCG↓, both COL11A1 siRNA and RMF effectively suppressed tumor growth and lung metastasis, an effect reversed by ITGB1 agonist.
TumMeta↓,
ITGB1↓, suppress triple-negative breast cancer metastasis by inactivating the ITGB1/FAK/YAP signaling pathway
FAK↓,
YAP/TEAD↓,
Dose↝, we selected two magnetic field frequencies (2.5 and 5 Hz) and three magnetic induction intensities (0.04, 0.2, and 0.41 T) for investigation.

3083- RES,    Resveratrol suppresses breast cancer cell invasion by inactivating a RhoA/YAP signaling axis
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, MDA-MB-468
YAP/TEAD↓, we demonstrate that resveratrol decreases the expression of YAP target genes
Rho↓, Strikingly, we also demonstrate that resveratrol inactivates RhoA, leading to the activation of Lats1 and induction of YAP phosphorylation.
FAK↓, REV decreases breast cancer cell invasion by inhibiting FAK,44 Rac and Cdc4245 activities
MMP9↓, REV has been shown to downregulate MMP-9 expression
ChemoSen↑, REV enhances the anticancer effects of doxorubicin in breast cancer cells
RAS↓, we reported that REV suppresses LPA-induced EGF receptor activation and subsequent inhibition a Ras/RhoA/ROCK signaling in ovarian cancer cells
ROCK1↓,
TumCI↓, REV may be used to reduce invasion and metastasis of breast cancer cells to improve outcomes for this devastating disease.
TumMeta↓,

3288- SIL,    Silymarin in cancer therapy: Mechanisms of action, protective roles in chemotherapy-induced toxicity, and nanoformulations
- Review, Var, NA
Inflam↓, Silymarin, a milk thistle extract, has anti-inflammatory, immunomodulatory, anti-lipid peroxidative, anti-fibrotic, anti-oxidative, and anti-proliferative properties.
lipid-P↓,
TumMeta↓, Silymarin exhibits not only anti-cancer functions through modulating various hallmarks of cancer, including cell cycle, metastasis, angiogenesis, apoptosis, and autophagy, by targeting a plethora of molecules
angioG↓,
chemoP↑, but also plays protective roles against chemotherapy-induced toxicity, such as nephrotoxicity,
EMT↓, Figure 2, Metastasis
HDAC↓,
HATs↑,
MMPs↓,
uPA↓,
PI3K↓,
Akt↓,
VEGF↓, Angiogenesis
CD31↓,
Hif1a↓,
VEGFR2↓,
Raf↓,
MEK↓,
ERK↓,
BIM↓, apoptosis
BAX↑,
Bcl-2↓,
Bcl-xL↓,
Casp↑,
MAPK↓,
P53↑,
LC3II↑, Autophagy
mTOR↓,
YAP/TEAD↓,
*BioAv↓, Additionally, the oral bioavailability of silymarin in rats is only 0.73 %
MMP↓, silymarin treatment reduced mitochondrial transmembrane potential, leading to an increase in cytosolic cytochrome c (Cyt c), downregulating proliferation-associated proteins (PCNA, c-Myc, cyclin D1, and β-catenin)
Cyt‑c↑,
PCNA↓,
cMyc↓,
cycD1/CCND1↓,
β-catenin/ZEB1↓,
survivin↓, and anti-apoptotic proteins (survivin and Bcl-2), and upregulating pro-apoptotic proteins (caspase-3, Bax, APAF-1, and p53)
APAF1↑,
Casp3↑,
MDSCs↓, ↓MDSCs, ↓IL-10, ↑IL-2 and IFN-γ
IL10↓,
IL2↑,
IFN-γ↑,
hepatoP↑, Moreover, in a randomized clinical trial, silymarin attenuated hepatoxicity in non-metastatic breast cancer patients undergoing a doxorubicin/cyclophosphamide-paclitaxel regimen
cardioP↑, For example, Rašković et al. studied the hepatoprotective and cardioprotective effects of silymarin (60 mg/kg orally) in rats following DOX
GSH↑, silymarin could protect the kidney and heart from ADR toxicity by protecting against glutathione (GSH) depletion and inhibiting lipid peroxidation
neuroP↑, silymarin attenuated the neurotoxicity of docetaxel by reducing apoptosis, inflammation, and oxidative stress

2234- SK,    Shikonin Suppresses Cell Tumorigenesis in Gastric Cancer Associated with the Inhibition of c-Myc and Yap-1
- in-vitro, GC, NA
TumCP↓, proliferation rate, migration, and invasion ability of the gastric cancer cell group decreased significantly after shikonin intervention for 24h
TumCI↓,
TumCMig↓,
cMyc↓, expression levels of c-Myc and Yap-1 in gastric cancer cells were found to be significantly decreased after shikonin intervention
YAP/TEAD↓,

3107- VitC,    Repurposing Vitamin C for Cancer Treatment: Focus on Targeting the Tumor Microenvironment
- Review, Var, NA
Risk↓, VitC supplementation resulted in dose-dependent reductions in all-cause mortality and the risk of various cancers
*ROS↓, Vitamin C (VitC) at the physiological dose (μM) is known to exhibit antioxidant properties.
ROS↑, However, it functions as a prooxidant at the pharmacological dose (mM) achieved by intravenous administration.
VEGF↓, VitC suppressed tumor angiogenesis in colon cancer-bearing mice by downregulating the expression and secretion of VEGF-A and VEGF-D
COX2↓, VitC impairs COX-2 activity and inhibits VEGF mRNA expression in melanoma cells in a time-dependent manner
ER Stress↑, VitC increases the ER stress-mediated breast cancer apoptosis via activation of the IRE-JNK-CHOP signaling pathway, an effect independent of ROS
IRE1↑,
JNK↑,
CHOP↑,
Hif1a↓, On the one hand, VitC directly inhibits HIF-1α-mediated glycolysis-related genes expression and the downstream acidic metabolites
eff↑, ROS generated by VitC treatment exerts a synergistic effect with other glycolysis inhibitors, providing a combined therapeutic strategy
Glycolysis↓,
MMPs↓, VitC inhibits a variety of metalloproteinases (MMPs) mRNA, which degrade ECM and release growth factors that drive tumor metastasis
TumMeta↓,
YAP/TEAD↓, VitC treatment reduces YAP1 expression while upregulating SYNPO-2; therefore, inhibiting metastasis of TNBC
eff↑, VitC enhances the killing efficiency of Hep G2 cells by low-dose sorafenib in vitro.
TET1↑, VitC stimulation of TET2 activity in the renal cell carcinoma


Showing Research Papers: 1 to 10 of 10

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 10

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GSH↑, 1,   HO-1↓, 1,   lipid-P↓, 1,   NRF2↓, 1,   NRF2↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   MEK↓, 1,   MMP↓, 1,   Raf↓, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 3,   p‑cMyc↑, 1,   Glycolysis↓, 1,  

Cell Death ⓘ

Akt↓, 3,   APAF1↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   Bcl-xL↓, 1,   BIM↓, 1,   Casp↑, 1,   Casp3↑, 1,   cl‑Casp3↑, 1,   cl‑Casp8↑, 1,   cl‑Casp9↑, 1,   Cyt‑c↑, 1,   DR5↑, 1,   Ferroptosis↑, 1,   Hippo↓, 1,   hTERT/TERT↓, 1,   iNOS↓, 1,   JNK↑, 2,   MAPK↓, 1,   MDM2↓, 1,   NICD↓, 1,   survivin↓, 2,   Telomerase↓, 1,   YAP/TEAD↓, 10,  

Transcription & Epigenetics ⓘ

HATs↑, 1,  

Protein Folding & ER Stress ⓘ

CHOP↑, 1,   ER Stress↑, 2,   IRE1↑, 1,  

Autophagy & Lysosomes ⓘ

LC3B-II↑, 1,   LC3II↑, 1,   TumAuto↑, 2,  

DNA Damage & Repair ⓘ

DNAdam↑, 1,   P53↑, 2,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CycB/CCNB1↓, 1,   cycD1/CCND1↓, 2,   P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

CD133↓, 1,   CD44↓, 1,   CSCs↑, 1,   EMT↓, 2,   ERK↓, 2,   p‑GSK‐3β↓, 1,   HDAC↓, 1,   MSCmark↓, 1,   mTOR↓, 2,   Nanog↓, 1,   NOTCH1↓, 1,   OCT4↓, 1,   PI3K↓, 2,   RAS↓, 2,   STAT3↓, 1,   TAZ↓, 3,   TumCG↓, 3,   Wnt↓, 1,  

Migration ⓘ

AEG1↓, 1,   Ca+2↑, 1,   CD31↓, 1,   COL11A1↓, 1,   E-cadherin↑, 1,   EM↑, 1,   FAK↓, 2,   ITGB1↓, 1,   MMP2↓, 1,   MMP9↓, 3,   MMPs↓, 2,   N-cadherin↓, 2,   Rho↓, 1,   ROCK1↓, 1,   TET1↑, 1,   TIMP1↑, 1,   TIMP2↑, 1,   TumCI↓, 3,   TumCMig↓, 2,   TumCP↓, 3,   TumCP↑, 1,   TumMeta↓, 4,   uPA↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 3,   Hif1a↓, 2,   VEGF↓, 3,   VEGFR2↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 2,   CXCR4↓, 1,   IFN-γ↓, 1,   IFN-γ↑, 1,   IL10↓, 1,   IL2↑, 1,   Inflam↓, 1,   MDSCs↓, 1,   NF-kB↓, 1,   p‑NF-kB↑, 1,   PD-L1↓, 1,  

Hormonal & Nuclear Receptors ⓘ

AR↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↓, 1,   ChemoSen↑, 3,   Dose↝, 1,   eff↑, 4,   MDR1↓, 1,   RadioS↑, 1,  

Clinical Biomarkers ⓘ

AR↓, 1,   hTERT/TERT↓, 1,   PD-L1↓, 1,  

Functional Outcomes ⓘ

cardioP↑, 1,   chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   Risk↓, 1,  
Total Targets: 127

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   ROS↓, 1,  

Metal & Cofactor Biology ⓘ

IronCh↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↓, 2,   BioAv↑, 1,  

Functional Outcomes ⓘ

toxicity↓, 1,  
Total Targets: 6

Scientific Paper Hit Count for: YAP/TEAD, YAP/TEAD activity
2 Luteolin
1 Artemisinin
1 Bufalin/Huachansu
1 Melatonin
1 Magnetic Field Rotating
1 Resveratrol
1 Silymarin (Milk Thistle) silibinin
1 Shikonin
1 Vitamin C (Ascorbic Acid)
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

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