PFK2 Cancer Research Results

PFK2, PFK2: Click to Expand ⟱
Source:
Type:
“PFK-2” typically refers to the family of bifunctional enzymes (commonly known as 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatases or PFKFBs) that regulate the levels of fructose-2,6-bisphosphate—a critical allosteric activator of glycolysis.

– PFK-2 enzymes catalyze the synthesis of fructose-2,6-bisphosphate (F2,6BP), which in turn is a potent activator of phosphofructokinase-1 (PFK-1), a key rate-limiting enzyme in glycolysis.
– Increased activity of PFK-2 contributes to enhanced glycolysis and the diversion of glycolytic intermediates into biosynthetic pathways that support rapid tumor cell growth and proliferation. – Upregulated glycolysis supports not only energy production but also the generation of precursors needed for nucleotide, amino acid, and lipid synthesis, aiding tumor progression.

– Elevated expression of certain PFK-2 isoforms (notably PFKFB3) has been observed in various cancers such as breast, colorectal, lung, and others.
– High PFK-2 expression is frequently associated with increased glycolytic activity, enhanced cell proliferation, and a shift toward an anabolic phenotype, correlating with more aggressive tumor behavior.
Scientific Papers found: Click to Expand⟱
1576- Citrate,    Targeting citrate as a novel therapeutic strategy in cancer treatment
- Review, Var, NA
TCA↓, Citrate serves as a key metabolite in the tricarboxylic acid cycle (TCA cycle, also referred to as the Krebs cycle)
T-Cell↝, modulation of T cell differentiation
Glycolysis↓, Citrate directly suppresses both cell glycolysis and TCA.
PKM2↓, citrate also inhibits glycolysis via its indirect inhibition of PK
PFK2?, In addition, citrate can inhibit PFK2,
SDH↓, citrate can inhibit enzymes, such as succinate dehydrogenase (SDH) and pyruvate dehydrogenase (PDH), in the TCA cycle
PDH↓,
β-oxidation↓, Citrate also inhibits β-oxidation as it promotes the formation of malonyl-CoA, which decreases the mitochondrial transport of fatty acids by inhibiting carnitine palmitoyl transferase I (CPT I)
CPT1A↓,
FASN↑, citrate has a positive role in promoting fatty acid synthesis
Casp3↑,
Casp2↑,
Casp8↑,
Casp9↑,
cl‑PARP↑,
Hif1a↓, Notably, in AML cell line U937, citrate induces apoptosis in a dose- and time-dependent manner by regulating the expression of HIF-1α and its downstream target GLUT-1
GLUT1↓,
angioG↓, citrate can also inhibit angiogenesis
Ca+2↓, chelate calcium ions in tumor cells
ROS↓, The other potential mechanism involved in citrate-mediated promotion of cancer growth and proliferation may be through its ability to decrease the levels of reactive oxygen species (ROS) in tumor cells
eff↓, dual effects of citrate in tumors may depend on the concentrations of citrate treatment, and different concentrations may bring out completely opposite effects even in the same tumor.
Dose↓, citrate concentration (<5 mM) appears to boost tumor growth and expansion in lung cancer A549 cells. 10mM and higher inhibited cell growth.
eff↑, citrate combined with ultraviolet (UV) radiation caused activation of caspase-3 and -9 in tumor cells (
Mcl-1↓, citrate has also been found to downregulate Mcl-1
HK2↓, Citrate also inhibits the enzymes PFK1 and hexokinase II (HK II) in glycolysis in tumor cells
IGF-1R↓,
PTEN↑, citrate may exert its effect via activating PTEN pathway
citrate↓, In addition to prostate cancer, citrate levels are significantly decreased in blood of patients with lung, bladder, pancreas and esophagus cancers
Dose∅, daily oral administration of citrate for 7 weeks at dose of 4 g/kg/day reduces tumor growth of several xenograft tumors and increases significantly the numbers of tumor-infiltrating T cells with no significant side effects in mouse models
eff↑, combining citrate with other compounds such as celecoxib, cisplatin, and 3-bromo-pyruvate, and have generated promising results
eff↑, combination of low effective doses of 3-bromo-pyruvate (3BP) (15uM), an inhibitor of glycolysis, and citrate (3 mM) significantly depleted the proliferation capability and migratory power of the C6 glioma
eff↑, Zinc treatment could lead to citrate accumulation in malignant prostate cells, which could have therapeutic potential in clinical therapy of prostate cancer.
eff↑, synergistic efficacy mediated by citrate combined with current checkpoint blockade therapies with anti-CTLA4 and/or anti-PD1/PDL1 will develop alternative novel strategies for future immunotherapy.


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 ⓘ

SDH↓, 1,  

Core Metabolism/Glycolysis ⓘ

citrate↓, 1,   CPT1A↓, 1,   FASN↑, 1,   Glycolysis↓, 1,   HK2↓, 1,   PDH↓, 1,   PFK2?, 1,   PKM2↓, 1,   TCA↓, 1,   β-oxidation↓, 1,  

Cell Death ⓘ

Casp2↑, 1,   Casp3↑, 1,   Casp8↑, 1,   Casp9↑, 1,   Mcl-1↓, 1,  

DNA Damage & Repair ⓘ

cl‑PARP↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

IGF-1R↓, 1,   PTEN↑, 1,  

Migration ⓘ

Ca+2↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Immune & Inflammatory Signaling ⓘ

T-Cell↝, 1,  

Drug Metabolism & Resistance ⓘ

Dose↓, 1,   Dose∅, 1,   eff↓, 1,   eff↑, 5,  
Total Targets: 29

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: PFK2, PFK2
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#:1144  State#:%  Dir#:0
  wNotes=on  sortOrder:rid,rpid

 

Home Page