Hif1a Cancer Research Results

Hif1a, HIF1α/HIF1a: Click to Expand ⟱
Source:
Type:
Hypoxia-Inducible-Factor 1A (HIF1A gene, HIF1α, HIF-1α protein product)
-Dominantly expressed under hypoxia(low oxygen levels) in solid tumor cells
-HIF1A induces the expression of vascular endothelial growth factor (VEGF)
-High HIF-1α expression is associated with Poor prognosis
-Low HIF-1α expression is associated with Better prognosis

-Functionally, HIF-1α is reported to regulate glycolysis, whilst HIF-2α regulates genes associated with lipoprotein metabolism.
-Cancer cells produce HIF in response to hypoxia in order to generate more VEGF that promote angiogenesis

Key mediators of aerobic glycolysis regulated by HIF-1α.
-GLUT-1 → regulation of the flux of glucose into cells.
-HK2 → catalysis of the first step of glucose metabolism.
-PKM2 → regulation of rate-limiting step of glycolysis.
-Phosphorylation of PDH complex by PDK → blockage of OXPHOS and promotion of aerobic glycolysis.
-LDH (LDHA): Rapid ATP production, conversion of pyruvate to lactate;

HIF-1α Inhibitors:
-Curcumin: disruption of signaling pathways that stabilize HIF-1α (ie downregulate).
-Resveratrol: downregulate HIF-1α protein accumulation under hypoxic conditions.
-EGCG: modulation of upstream signaling pathways, leading to decreased HIF-1α activity.
-Emodin: reduce HIF-1α expression. (under hypoxia).
-Apigenin: inhibit HIF-1α accumulation.
Bladder, Bladder Cancer: Click to Expand ⟱
Bladder Cancer
Scientific Papers found: Click to Expand⟱
1214- VitK2,    Vitamin K2 promotes PI3K/AKT/HIF-1α-mediated glycolysis that leads to AMPK-dependent autophagic cell death in bladder cancer cells
- in-vitro, Bladder, T24/HTB-9 - in-vitro, Bladder, J82
Glycolysis↑, GlucoseCon↑, lactateProd↑, TCA↓, PI3K↑, Akt↑, AMPK↑, mTORC1↓, TumAuto↑, GLUT1↑, HK2↑, LDHA↑, ACC↓, PDH↓, eff↓, cMyc↓, Hif1a↑, p‑Akt↑, eff↓, eff↓, eff↓, eff↓, ROS↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

ROS↑, 1,  

Core Metabolism/Glycolysis ⓘ

ACC↓, 1,   AMPK↑, 1,   cMyc↓, 1,   GlucoseCon↑, 1,   Glycolysis↑, 1,   HK2↑, 1,   lactateProd↑, 1,   LDHA↑, 1,   PDH↓, 1,   TCA↓, 1,  

Cell Death ⓘ

Akt↑, 1,   p‑Akt↑, 1,  

Autophagy & Lysosomes ⓘ

TumAuto↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTORC1↓, 1,   PI3K↑, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↑, 1,  

Barriers & Transport ⓘ

GLUT1↑, 1,  

Drug Metabolism & Resistance ⓘ

eff↓, 5,  
Total Targets: 19

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Hif1a, HIF1α/HIF1a
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:32  Cells:%  prod#:%  Target#:143  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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