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⟱
684- EGCG,    Improving the anti-tumor effect of EGCG in colorectal cancer cells by blocking EGCG-induced YAP activation
- in-vitro, CRC, NA
eff↑, YAP blockade increases the sensitivity of CRC cells to EGCG treatment
Akt↓,
VEGFR2↓,
STAT3↓,
P53↓,
Hippo↓,
YAP/TEAD↑, activates downstream YAP : Activation of YAP impedes the anti-tumor effects of EGCG

6419- MEL,    The potential influence of melatonin on mitochondrial quality control: a review
- Review, Nor, NA
*mt-ACC⇅, Melatonin regulates pyruvate or fatty acid metabolism to increase the concentration of acetyl-CoA in mitochondria. these studies indicate that melatonin increases or decreases acetyl-CoA content in mitochondria to regulate mitochondrial metabolism.
*PKM1↑, melatonin increases the activity of pyruvate kinase M1/2 (PKM) to regulate glycolysis
*PKM2↑,
*Glycolysis↝,
*PDKs↑, melatonin activates pyruvate dehydrogenase kinase 4 (PDK4) to regulate acetyl-CoA content
*FAO↑, melatonin can promote fatty acid metabolism by directly enhancing β-oxidation or increasing the transfer of fatty acid-derived acetyl-CoA into mitochondria
*ETC↑, Second, melatonin can enhance the activity of the electron-transport chain (ETC) and oxidative phosphorylation (OXPHOS) to regulate mitochondrial metabolism.
*OXPHOS↑,
*ATP↑, melatonin enhanced OXPHOS and promoted adenosine triphosphate (ATP) synthesis in rat brain and liver mitochondria
Glycolysis↓, ome studies have found that melatonin drove the switch from cytosolic glycolysis to mitochondrial OXPHOS in cancer cells
OXPHOS↑,
*Ca+2↓, melatonin can regulate the membrane potential of mitochondria and decrease excessive calcium levels to enhance ETC activity to increase ATP production
*ROS↓, Melatonin exhibits superior antioxidant ability. Melatonin, as a major scavenger of reactive oxygen species (ROS), may play a pivotal role in protecting mitochondria from ROS-induced injury
*antiOx↑, These specific characteristics make melatonin a broad-spectrum antioxidant.
*SOD2↑, melatonin can upregulate the expression of superoxide dismutase (MnSOD), glutathione peroxidase (GSH-Px) and catalase (CAT) to prevent cell stress and injury
*GPx↑,
*Catalase↑,
*MFN1↑, On the one hand, melatonin increases mitochondrial fusion-related genes such as mitofusin-1 (Mfn1), mitofusin-2 (Mfn2) and optic atrophy1 (Opa1) to promote mitochondrial fusion
*MFN2↑,
*OPA1↑,
*YAP/TEAD↑, studies have found that melatonin activated the Yap-Hippo pathway to increase Opa1-related fusion
*Hippo↑,
*SIRT1↑, melatonin alleviated cardiac dysfunction induced by diabetes by upregulating SIRT1-PGC1α to inhibit the expression of Drp1
*PGC-1α↑,
*DRP1/DNM1L↓,

2247- MF,    Effects of Pulsed Electromagnetic Field Treatment on Skeletal Muscle Tissue Recovery in a Rat Model of Collagenase-Induced Tendinopathy: Results from a Proteome Analysis
- in-vivo, Nor, NA
*Glycolysis↓, PEMF-treated animals exhibited decreased glycolysis and increased LDHB expression, enhancing NAD signaling and ATP production
*LDHB↑,
*NAD↑,
*ATP↑,
*antiOx↑, Antioxidant protein levels increased, controlling ROS production.
*ROS↑,
*YAP/TEAD↑, upregulation of YAP and PGC1alpha and increasing slow myosin isoforms, thus speeding up physiological recovery.
*PGC-1α↑,
*TCA↑, increased in PEMF-treated injured limbs
*FAO↑,
*OXPHOS↑, Oxidative phosphorylation was increased in the muscle of injured rats that underwent PEMF treatment

1751- WBV,    Yoda1 Enhanced Low-Magnitude High-Frequency Vibration on Osteocytes in Regulation of MDA-MB-231 Breast Cancer Cell Migration
- in-vitro, BC, MDA-MB-231 - in-vitro, AML, RAW264.7
BMD↑, Low-magnitude (≤1 g) high-frequency (≥30 Hz) (LMHF) vibration has been shown to enhance bone mineral density
YAP/TEAD↑, Combined treatment on osteocytes showed beneficial effects, including increasing the nuclear translocation of Yes-associated protein (YAP) in osteocytes
TumCG↓, The ability of carefully controlled high-magnitude mechanical loads to suppress breast cancer growth and maintain bone integrity has been shown using various models in vivo
Strength↑, Studies have shown the anabolic benefits of LMHF vibration (LMHFV) on the musculoskeletal system, including increased bone density [7], reduced marrow fat [8], and improved muscle and glucose metabolism
TumCI↓, Application of LMHF vibration on MDA-MB-231 cells does not affect their migration [25], cell viability, and apoptosis but suppresses their invasion and upregulates FAS, a membrane death receptor
Fas↑,
Ca+2↑, concentration of intracellular calcium in MLO-Y4 was shown to significantly increase after 90 Hz of vibration for 1 h


Showing Research Papers: 1 to 4 of 4

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 4

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

OXPHOS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Fas↑, 1,   Hippo↓, 1,   YAP/TEAD↑, 2,  

DNA Damage & Repair(tgid=10) ⓘ

P53↓, 1,  

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

STAT3↓, 1,   TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ca+2↑, 1,   TumCI↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

VEGFR2↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BMD↑, 1,  

Functional Outcomes(tgid=23) ⓘ

Strength↑, 1,  
Total Targets: 15

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   Catalase↑, 1,   GPx↑, 1,   MFN1↑, 1,   MFN2↑, 1,   OPA1↑, 1,   OXPHOS↑, 2,   ROS↓, 1,   ROS↑, 1,   SOD2↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

ATP↑, 2,   DRP1/DNM1L↓, 1,   ETC↑, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

mt-ACC⇅, 1,   FAO↑, 2,   Glycolysis↓, 1,   Glycolysis↝, 1,   LDHB↑, 1,   NAD↑, 1,   PDKs↑, 1,   PKM1↑, 1,   PKM2↑, 1,   SIRT1↑, 1,   TCA↑, 1,  

Cell Death(tgid=5) ⓘ

Hippo↑, 1,   YAP/TEAD↑, 2,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,  
Total Targets: 28

Scientific Paper Hit Count for: YAP/TEAD, YAP/TEAD activity
1 EGCG (Epigallocatechin Gallate)
1 Melatonin
1 Magnetic Fields
1 Whole Body Vibration
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:340  State#:%  Dir#:2
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