PKM2:PKM1 Cancer Research Results

PKM2:PKM1, PKM2/PKM1 ratio: Click to Expand ⟱
Source:
Type:
PKM2/PKM1 ratio
-PKM (pyruvate kinase M) exists mainly as two splice isoforms: PKM1 and PKM2.
-PKM1 is constitutively active and typically found in tissues with high-energy demands (e.g., muscle, brain).
-PKM2 is less active under some conditions and is highly regulated; importantly, it is often upregulated in cancers.
- A higher PKM2/PKM1 ratio is thought to promote the “Warburg effect” (aerobic glycolysis) that benefits rapidly proliferating tumor cells by providing biosynthetic precursors even though it is less energy efficient.
-An increased PKM2/PKM1 ratio has been associated with enhanced tumor cell proliferation, survival, and metastasis.
Scientific Papers found: Click to Expand⟱
2314- Api,    Apigenin Restrains Colon Cancer Cell Proliferation via Targeted Blocking of Pyruvate Kinase M2-Dependent Glycolysis
- in-vitro, Colon, HCT116 - in-vitro, Colon, HT29 - in-vitro, Colon, DLD1
Glycolysis↓, AP could block cellular glycolysis through restraining the tumor-specific pyruvate kinase M2 (PKM2) activity and expression and further significantly induce anti-colon cancer effects.
PKM2:PKM1↓,
β-catenin/ZEB1↓, AP decreases the expression of PKM2 in HCT116 by blocking the B-catenin/c-Myc /PTBP1 pathway
cMyc↓,

2313- Flav,    Flavonoids against the Warburg phenotype—concepts of predictive, preventive and personalised medicine to cut the Gordian knot of cancer cell metabolism
- Review, Var, NA
Warburg↓, Flavonoids modulate key pathways involved in the Warburg phenotype including but not limited to PKM2, HK2, GLUT1 and HIF-1.
antiOx↑, Flavonoids represent a diverse group of phytochemicals (Fig. 3) that exhibit antioxidative, antiangiogenic and overall antineoplastic efficacy
angioG↓,
Glycolysis↓, Apigenin (AP) blocked glycolysis through regulation of PKM2 activity and expression in a colon cancer cell line (HCT116)
PKM2↓,
PKM2:PKM1↓, AP is regarded as a potential allosteric inhibitor of PKM2. AP could maintain a low PKM2/PKM1 ratio as a consequence of inhibition of the β-catenin/c-Myc/PTBP1 pathway
β-catenin/ZEB1↓,
cMyc↓,
HK2↓, QUE reduced the level of HK2 and suppressed Akt/mTOR signalling in hepatocellular cancer lines (SMMG-7721, BEL-7402) in vitro.
Akt↓,
mTOR↓,
GLUT1↓, EGCG demonstrated anticancer efficacy against 4T1 via reduction of GLUT1 expression
Hif1a↓, BA suppressed glycolysis via PTEN/Akt/HIF-1α, it is a possible therapeutic sensitiser against gastric cancer


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:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Core Metabolism/Glycolysis ⓘ

cMyc↓, 2,   Glycolysis↓, 2,   HK2↓, 1,   PKM2↓, 1,   PKM2:PKM1↓, 2,   Warburg↓, 1,  

Cell Death ⓘ

Akt↓, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,  

Migration ⓘ

β-catenin/ZEB1↓, 2,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  
Total Targets: 13

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PKM2:PKM1, PKM2/PKM1 ratio
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#:1291  State#:%  Dir#:1
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