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.
NSCLC, Non-small Cell Lung Cancer: Click to Expand ⟱
Non-small Cell Lung Cancer
Scientific Papers found: Click to Expand⟱
5180- BBR,    Berberine Targets AP-2/hTERT, NF-κB/COX-2, HIF-1α/VEGF and Cytochrome-c/Caspase Signaling to Suppress Human Cancer Cell Growth
- in-vitro, NSCLC, NA
TumCMig↓, TumCP↓, Apoptosis↑, TFAP2A↓, hTERT/TERT↓, NF-kB↓, COX2↓, Hif1a↓, VEGF↓, Akt↓, p‑ERK↓, Cyt‑c↑, cl‑Casp↑, cl‑PARP↑, PI3K↓, Akt↓, Raf↓, MEK↓, ERK↓,
4505- GLA,    Gamma linolenic acid suppresses hypoxia-induced proliferation and invasion of non-small cell lung cancer cells by inhibition of HIF1α
- in-vitro, NSCLC, Calu-1
TumCP↓, PCNA↓, Ki-67↓, MCM2↓, Bcl-2↓, BAX↑, cl‑Casp3↑, TumCMig↓, TumCI↓, Hif1a↓, VEGF↓,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Mitochondria & Bioenergetics ⓘ

MEK↓, 1,   Raf↓, 1,  

Cell Death ⓘ

Akt↓, 2,   Apoptosis↑, 1,   BAX↑, 1,   Bcl-2↓, 1,   cl‑Casp↑, 1,   cl‑Casp3↑, 1,   Cyt‑c↑, 1,   hTERT/TERT↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

TFAP2A↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

ERK↓, 1,   p‑ERK↓, 1,   MCM2↓, 1,   PI3K↓, 1,  

Migration ⓘ

Ki-67↓, 1,   TumCI↓, 1,   TumCMig↓, 2,   TumCP↓, 2,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,   VEGF↓, 2,  

Immune & Inflammatory Signaling ⓘ

COX2↓, 1,   NF-kB↓, 1,  

Clinical Biomarkers ⓘ

hTERT/TERT↓, 1,   Ki-67↓, 1,  
Total Targets: 27

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:19  Cells:%  prod#:%  Target#:143  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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