PFKFB2 Cancer Research Results

PFKFB2, 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase 2: Click to Expand ⟱
Source:
Type:
PFKFB2 (6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase 2) is one of the isoenzymes responsible for regulating the intracellular levels of fructose-2,6-bisphosphate, a key activator of phosphofructokinase-1 (PFK-1) in glycolysis. Its role in cancer metabolism is of increasing interest due to its involvement in regulating glycolytic flux.

• In many cancers, increased glycolytic activity is a hallmark. Upregulation of PFKFB2 in some tumors can contribute to this metabolic reprogramming, although expression patterns may be context- and tissue-specific.

• Both upregulation and, in some settings, downregulation have been reported, reflecting the enzyme’s complex involvement in metabolic regulation and potential feedback mechanisms within the tumor microenvironment.

• Some studies have correlated high PFKFB2 expression with aggressive tumor characteristics, such as increased proliferation, enhanced glycolysis, and potentially poorer clinical outcomes.

• In certain cancers, elevated levels of PFKFB2 may indicate a metabolic phenotype that favors tumor growth and resistance to stress, potentially serving as a marker of poor prognosis.
Scientific Papers found: Click to Expand⟱
7286- GGB,    Ginsenoside Rh2 shifts tumor metabolism from aerobic glycolysis to oxidative phosphorylation through regulating the HIF1-α/PDK4 axis in non-small cell lung cancer
- in-vitro, Lung, A549 - in-vitro, Lung, PC9
Hif1a↓, G-Rh2 could target and down-regulate the expression of HIF-1α, resulting in decreased expression of glycolytic enzymes and inhibition of aerobic glycolysis in tumors.
Glycolysis↓,
OXPHOS↑, directly targeting mitochondrial PDK, it elevated mitochondrial oxidative phosphorylation and enhanced ROS accumulation, thereby promoting tumor cells to undergo normal apoptotic processes.
ROS↑,
Apoptosis↑,
toxicity↓, intraperitoneal administration of 20 mg/kg G-Rh2 didn’t decrease the weights of the mice, thus suggesting that 20 mg/kg G-Rh2 was non-toxic.
PDKs↓, G-Rh2 inhibited the expression of PDK4 (
HK2↓, G-Rh2 treatment downregulated the expression of of the expression of glycolysis-related proteins HK2, LDHA, PFKFB2, and PKM2
LDHA↓,
PFKFB2↓,
PKM2↓,
eff↑, It could act synergistically with lower doses of DCA to inhibit both sites of PDK, acting as a potentiator and detoxifier.

2444- SFN,    Sulforaphane Delays Fibroblast Senescence by Curbing Cellular Glucose Uptake, Increased Glycolysis, and Oxidative Damage
- in-vitro, Nor, MRC-5
*GlucoseCon↓, SFN delayed senescence by decreasing glucose metabolism on the approach to senescence, exhibiting a caloric restriction mimetic-like activity
*ROS↓, and thereby decreased oxidative damage to cell protein and DNA
*Trx↓, This was associated with increased expression of thioredoxin-interacting protein, curbing entry of glucose into cells;
*HK2↓, decreased hexokinase-2
*NRF2↑, SFN is an activator of transcription factor Nrf2 [14] which regulates antioxidant response element- (ARE-) linked gene expression.
*Catalase↑, CAT, PDRX1, and GCLM, expression was increased in senescence and treatment with SFN increased the expression further
*TXNIP↑, increased expression of TXNIP, curbing the entry of glucose into cells
*PFKFB2↓, decreased PFKFB2 and increased G6PD, downregulating glycolysis.
*G6PD↑,

2417- SK,    Shikonin inhibits the Warburg effect, cell proliferation, invasion and migration by downregulating PFKFB2 expression in lung cancer
- in-vitro, Lung, A549 - in-vitro, Lung, H446
TumCP↓, Shikonin treatment decreased the proliferation, migration, invasion, glucose uptake, lactate levels, ATP levels and PFKFB2 expression levels and increased apoptosis in lung cancer cells in a dose‑dependent manner.
TumCMig↓,
TumCI↓,
GlucoseCon↓,
lactateProd↓,
PFKFB2↓,
Warburg↓, shikonin inhibited the Warburg effect and exerted antitumor activity in lung cancer cells, which was associated with the downregulation of PFKFB2 expression.
GLUT1∅, while the expression levels of the other proteins (PDK1, GLUT1, PGK2, LDHA, PKM2, GLUT3, PDH and p-PDH) were not altered by shikonin treatment.
LDHA∅,
PKM2∅,
GLUT3∅,
PDH∅,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

OXPHOS↑, 1,   ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   LDHA↓, 1,   LDHA∅, 1,   PDH∅, 1,   PDKs↓, 1,   PFKFB2↓, 2,   PKM2↓, 1,   PKM2∅, 1,   Warburg↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,  

Migration(tgid=13) ⓘ

TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1∅, 1,   GLUT3∅, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,  

Functional Outcomes(tgid=23) ⓘ

toxicity↓, 1,  
Total Targets: 23

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

Catalase↑, 1,   NRF2↑, 1,   ROS↓, 1,   Trx↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

G6PD↑, 1,   GlucoseCon↓, 1,   HK2↓, 1,   PFKFB2↓, 1,  

Migration(tgid=13) ⓘ

TXNIP↑, 1,  
Total Targets: 9

Scientific Paper Hit Count for: PFKFB2, 6-Phosphofructo-2-Kinase/Fructose-2,6-Bisphosphatase 2
1 Ginkgolide B
1 Sulforaphane (mainly Broccoli)
1 Shikonin
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#:1307  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

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