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.


ESCC, Oesophageal Squamous Cell Carcinoma: Click to Expand ⟱
Esophageal cancer is a growth of cells that starts in the esophagus.


Scientific Papers found: Click to Expand⟱
957- ART/DHA,    Artemisinin inhibits the development of esophageal cancer by targeting HIF-1α to reduce glycolysis levels
- in-vitro, ESCC, KYSE150 - in-vitro, ESCC, KYSE170
TumCP↓, TumMeta↓, Glycolysis↓, N-cadherin↓, PKM2↓, Hif1a↓,
2289- Ba,  Rad,    Baicalein Inhibits the Progression and Promotes Radiosensitivity of Esophageal Squamous Cell Carcinoma by Targeting HIF-1A
- in-vitro, ESCC, KYSE150
TumCP↓, TumCMig↓, Glycolysis↓, cycD1/CCND1↓, CDK4↓, ECAR↓, TumCCA↑, HK1↓, ALDH↓, ALDOA↓, PKM2↓, Hif1a↓,
2194- SK,    Efficacy of Shikonin against Esophageal Cancer Cells and its possible mechanisms in vitro and in vivo
- in-vitro, ESCC, Eca109 - in-vitro, ESCC, EC9706 - in-vivo, NA, NA
tumCV↓, TumCCA↑, Apoptosis↑, EGFR↓, PI3K↓, Hif1a↓, PKM2↓, cycD1/CCND1↓, AntiTum↑,

Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress

HK1↓, 1,  

Core Metabolism/Glycolysis

ALDOA↓, 1,   ECAR↓, 1,   Glycolysis↓, 2,   PKM2↓, 3,  

Cell Death

Apoptosis↑, 1,  

Transcription & Epigenetics

tumCV↓, 1,  

Cell Cycle & Senescence

CDK4↓, 1,   cycD1/CCND1↓, 2,   TumCCA↑, 2,  

Proliferation, Differentiation & Cell State

ALDH↓, 1,   PI3K↓, 1,  

Migration

N-cadherin↓, 1,   TumCMig↓, 1,   TumCP↓, 2,   TumMeta↓, 1,  

Angiogenesis & Vasculature

EGFR↓, 1,   Hif1a↓, 3,  

Clinical Biomarkers

EGFR↓, 1,  

Functional Outcomes

AntiTum↑, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: Hif1a, HIF1α/HIF1a
1 Artemisinin
1 Baicalein
1 Radiotherapy/Radiation
1 Shikonin
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:41  Cells:%  prod#:%  Target#:143  State#:%  Dir#:1
wNotes=0 sortOrder:rid,rpid

 

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