PFK1 Cancer Research Results

PFK1, Phosphofructokinase-1: Click to Expand ⟱
Source:
Type:
Phosphofructokinase-1 (PFK1) is a key regulatory enzyme in glycolysis that catalyzes the conversion of fructose-6-phosphate to fructose-1,6-bisphosphate.
– As a rate-limiting enzyme in glycolysis, PFK1 is subject to complex regulation through allosteric effectors including ATP, AMP, and fructose-2,6-bisphosphate.
• Metabolic Control:
–PFK1 activity is central to controlling the pace of glycolysis, thereby influencing energy production and intermediary metabolite supply.
– In highly proliferative cells or cells under growth conditions, increased glycolytic flux (and, by extension, PFK1 activity) supports the biosynthetic demands of cell division.

– Many tumors (including breast, colorectal, and lung cancers) have been reported to have increased PFK1 expression/activity relative to normal tissues.
– High glycolytic flux, driven partly by enhanced PFK1, supports rapid cell proliferation and survival in the nutrient/stress-challenged tumor microenvironment.

Inhibitors:(typically glycolysis is targeted more broadly)
-Citrate
-Hydrogen ions (pH) – Acidic conditions can have inhibitory effects.
-3PO: inhibits PFKFB3, thereby indirectly reducing PFK1 activity.
-Resveratrol can downregulate glycolytic flux in cancer cells, which may indirectly affect PFK1 activity.
- FMDs offer an indirect strategy to modulate cancer metabolism by broadly reducing glycolysis. Their impact on PFK1 is likely part of a complex network of metabolic adaptations rather than a direct inhibitory effect.
Colon, Colon Cancer: Click to Expand ⟱
Colon cancer can start anywhere in the colon, (5 feet long) and absorbs water from stool. Rectal cancer starts in the rectum, which is the last 12 centimeters.
Scientific Papers found: Click to Expand⟱
1861- dietFMD,  Chemo,    Fasting induces anti-Warburg effect that increases respiration but reduces ATP-synthesis to promote apoptosis in colon cancer models
- in-vitro, Colon, CT26 - in-vivo, NA, NA
selectivity↑, ChemoSen↑, BG↓, AminoA↓, Warburg↓, OCR↑, ATP↓, ROS↑, Apoptosis↑, GlucoseCon↓, PI3K↓, PTEN↑, GLUT1↓, GLUT2↓, HK2↓, PFK1↓, PKA↓, ATP:AMP↓, Glycolysis↓, lactateProd↓,

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,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   OCR↑, 1,  

Core Metabolism/Glycolysis ⓘ

AminoA↓, 1,   ATP:AMP↓, 1,   GlucoseCon↓, 1,   GLUT2↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PFK1↓, 1,   Warburg↓, 1,  

Cell Death ⓘ

Apoptosis↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   PTEN↑, 1,  

Migration ⓘ

PKA↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 1,   selectivity↑, 1,  

Clinical Biomarkers ⓘ

BG↓, 1,  
Total Targets: 20

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PFK1, Phosphofructokinase-1
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:31  Cells:%  prod#:%  Target#:988  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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