ATPase Cancer Research Results
ATPase, ATPase (V‐ATPase): Click to Expand ⟱
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Vacuolar ATPase (V‐ATPase) is an ATP‐dependent H+‐transporter that pumps protons across intracellular and plasma membranes. V-ATPase inhibition reduces in vitro invasion and migration of a variety of cancer cell types and that the pump is involved in signaling, growth, survival, and drug resistance of cancer cells.
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Scientific Papers found: Click to Expand⟱
HSP90↓, Here, we investigated the mechanism by which capsaicin inhibits Hsp90
ATPase↓, capsaicin binds to the N-terminus of Hsp90 and inhibits its ATPase activity
eff↑, Combined treatments of capsaicin and the Hsp90 inhibitor 17-AAG improved the anti-tumor efficacy of 17-AAG in cell culture
HSP70/HSPA5↓, capsaicin triggers the lysosomal degradation of Hsp70 in various cancer cell lines
other↝, The mechanism by which capsaicin induces apoptosis in cancer cells is not well understood, but it appears to be independent of the TRPV1 receptor as neither capsazepine, a TRPV1 antagonist, nor intracellular Ca2+ chelators have been found to inhibit
NF-kB↓, capsaicin can block the activity of many oncogenic signaling proteins including NF-κB, ER, EGFR/HER2, CDK4, Src, VEGF, and PI3K/Akt, among others.
EGFR↓,
CDK4↓,
Src↓,
VEGF↓,
PI3K↓,
Akt↓,
TumCP↓, Celastrol affected the proliferation of U937 in a dose-dependent way, arresting the cell cycle at G0/G1 with 400 nM doses and triggering cell death with doses above 1000 nM.
TumCCA↑,
TumCD↑,
HSP90↓, Cell cycle arrest was accompanied by inhibition of HSP90 ATPase activity and elevation in HSP70 levels (a biochemical hallmark of HSP90 inhibition),
HSP70/HSPA5↑,
cycD1/CCND1↓, reduction in Cyclin D1, Cdk4 and Cdk6 levels
CDK4↓,
CDK6↓,
ATPase↓, celastrol's effects on ATPase activity in the protein complex pulled-down by anti-HSP90
P53↑, upregulated other targets including p53, death receptor (DR-5), JN-kinase, Nrf-2, and peroxisome proliferator-activated receptor γ (PPARγ) factors
DR5↑,
JNK↑,
NRF2↑,
PPARγ↑,
HER2/EBBR2↓, (Her-2, IR, ER-a, and Fas receptor)
IR↓,
ER(estro)↓,
Fas↑,
PDGF↓, (PDGF, TGF, FGF, and EGF)
TGF-β↓,
FGF↓,
EGFR↓,
JAK↓,
PAK↓,
MAPK↓,
ATPase↓, (ATPase, COX-2, and matrix metalloproteinase enzyme [MMP])
COX2↓,
MMPs↓,
IL1↓, inflammatory cytokines (IL-1, IL-2, IL-5, IL-6, IL-8, IL-12, and IL-18)
IL2↓,
IL5↓,
IL6↓,
IL8↓,
IL12↓,
IL18↓,
NF-kB↓,
NOTCH1↓,
STAT1↓,
STAT4↓,
STAT5↓,
STAT3↓,
Apoptosis↑,
Bcl-2↓,
P53↑, up-regulated expression of p53,
cl‑Casp3↑,
Cyt‑c↑,
ROS↑, induced ROS production by suppressing the expression of antioxidant regulatory enzymes, namely superoxide dismutase and catalase
SOD↓,
Catalase↓,
Glycolysis↓,
GLUT3↓,
LDHA↓, LDHA inhibitor
MCT1↓,
NHE1↓,
ATPase↓,
CAIX↓,
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 ⓘ
Catalase↓, 1, NRF2↑, 1, ROS↑, 1, SOD↓, 1,
Core Metabolism/Glycolysis ⓘ
CAIX↓, 1, Glycolysis↓, 1, IR↓, 1, LDHA↓, 1, PPARγ↑, 1,
Cell Death ⓘ
Akt↓, 1, Apoptosis↑, 1, Bcl-2↓, 1, cl‑Casp3↑, 1, Cyt‑c↑, 1, DR5↑, 1, Fas↑, 1, JNK↑, 1, MAPK↓, 1, MCT1↓, 1, TumCD↑, 1,
Kinase & Signal Transduction ⓘ
HER2/EBBR2↓, 1, PAK↓, 1,
Transcription & Epigenetics ⓘ
other↝, 1,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↓, 1, HSP70/HSPA5↑, 1, HSP90↓, 2,
DNA Damage & Repair ⓘ
P53↑, 2,
Cell Cycle & Senescence ⓘ
CDK4↓, 2, cycD1/CCND1↓, 1, TumCCA↑, 1,
Proliferation, Differentiation & Cell State ⓘ
FGF↓, 1, NOTCH1↓, 1, PI3K↓, 1, Src↓, 1, STAT1↓, 1, STAT3↓, 1, STAT4↓, 1, STAT5↓, 1,
Migration ⓘ
ATPase↓, 4, MMPs↓, 1, PDGF↓, 1, TGF-β↓, 1, TumCP↓, 1,
Angiogenesis & Vasculature ⓘ
EGFR↓, 2, VEGF↓, 1,
Barriers & Transport ⓘ
GLUT3↓, 1, NHE1↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1↓, 1, IL12↓, 1, IL18↓, 1, IL2↓, 1, IL5↓, 1, IL6↓, 1, IL8↓, 1, JAK↓, 1, NF-kB↓, 2,
Hormonal & Nuclear Receptors ⓘ
CDK6↓, 1, ER(estro)↓, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 1,
Clinical Biomarkers ⓘ
EGFR↓, 2, HER2/EBBR2↓, 1, IL6↓, 1,
Total Targets: 63
Pathway results for Effect on Normal Cells:
Total Targets: 0
Scientific Paper Hit Count for: ATPase, ATPase (V‐ATPase)
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#:364 State#:% Dir#:1
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