PFK Cancer Research Results
PFK, Phosphofructokinase: Click to Expand ⟱
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PFK (Phosphofructokinase) is a key enzyme in glycolysis, the process by which cells convert glucose into energy. PFK is overexpressed in many types of cancer, and its expression is often associated with poor prognosis.
Mechanisms:
• PFK promotes glycolysis, which is a key metabolic pathway in cancer cells.
• PFK helps to produce energy for cancer cells.
• PFK promotes cell proliferation.
Therapeutic Targeting:
• PFK inhibitors are being developed as a potential therapeutic strategy for cancer treatment.
• Inhibitors of glycolysis, such as 2-deoxyglucose, are being explored as a potential therapeutic strategy for cancer treatment.
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Scientific Papers found: Click to Expand⟱
*OS↑, MR seems to be an approach to prolong lifespan which has been validated extensively in various animal models
*mt-ROS↓, Mitochondrial ROS reduction by methionine restriction (MR) maintains redox balance
*H2S↑, MR ameliorates oxidative stress by autophagy activation and hepatic H2S generation.
*FGF21↑, MR impact on cognition by upregulation of FGF21 and alterations of gut microbiome.
*cognitive↑,
*GutMicro↑,
*IGF-1↓, long-term, low-fat, whole-food vegan diet may increase life expectancy in humans by down-regulating IGF-I activity
*mTOR↓, Suppression of the mTOR pathway by MR can also lead to increased H2S production,
*GSH↑, 80% MR increases the GSH content in erythrocytes of rats,
*SOD↑, A diet restricting methionine to 80% (0.17% Met) significantly increases plasma SOD and decreases MDA levels while increasing mRNA expression of Nrf2, HO-1, and NQO-1 in the heart of HFD-fed mice with cardiovascular impairment
*MDA↓,
*NRF2↑,
*HO-1↑,
*NQO1↑,
*GLUT4↑, In skeletal muscle, MR improved expression and transport of GLUT4 and glycogen levels and increased the expression of glycolysis-related genes (HK2, PFK, PKM) in HFD-fed mice
*Glycolysis↑,
*HK2↑,
*PFK↑,
*PKM2↑,
*GlucoseCon↑, promoting glucose uptake and glycogen synthesis, glycolysis, and aerobic oxidation in skeletal muscle.
*ATF4↑, MR can increase the expression of hepatic FGF21 by activating GCN2/ATF4/PPARα signaling in liver cells, thereby improving insulin sensitivity, accelerating energy expenditure, and promoting fat oxidation and glucose metabolism
*PPARα↑,
GSH↓, MR was able to decrease GSH in HepG2 cells, thereby regulating the activation state of protein tyrosine phosphatases such as PTEN.
GSTs↑, decrease of GSH by MR also triggers upregulation of glutathione S-transferase
ROS↑, Double deprivation of methionine and cystine both in vitro and in vivo resulted in a decrease in GSH content, an increase in ROS levels, and an induction of autophagy in glioma cells
*neuroP↑, A neuroprotective role of FGF21
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 ⓘ
GSH↓, 1, GSTs↑, 1, ROS↑, 1,
Total Targets: 3
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
GSH↑, 1, HO-1↑, 1, MDA↓, 1, NQO1↑, 1, NRF2↑, 1, mt-ROS↓, 1, SOD↑, 1,
Core Metabolism/Glycolysis ⓘ
FGF21↑, 1, GlucoseCon↑, 1, Glycolysis↑, 1, H2S↑, 1, HK2↑, 1, PFK↑, 1, PKM2↑, 1, PPARα↑, 1,
Proliferation, Differentiation & Cell State ⓘ
IGF-1↓, 1, mTOR↓, 1,
Angiogenesis & Vasculature ⓘ
ATF4↑, 1,
Barriers & Transport ⓘ
GLUT4↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1,
Functional Outcomes ⓘ
cognitive↑, 1, neuroP↑, 1, OS↑, 1,
Total Targets: 23
Scientific Paper Hit Count for: PFK, Phosphofructokinase
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#:945 State#:% Dir#:2
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