PFKP Cancer Research Results

PFKP, Phosphofructokinase, Platelet: Click to Expand ⟱
Source:
Type: enzyme
PFKP (Phosphofructokinase, Platelet) is an enzyme that plays a crucial role in glycolysis, the process by which cells convert glucose into energy. PFKP is a key regulatory enzyme in the glycolytic pathway, and it is primarily expressed in platelets and other hematopoietic cells.
PFKP has been shown to be overexpressed in certain types of tumors, including leukemia and lymphoma. This overexpression may contribute to the development and progression of cancer by promoting glycolysis and energy production in cancer cells.
PFKP is a key regulatory enzyme in the glycolytic pathway.
PFKP plays a role in the regulation of glucose metabolism in diabetes.
PFKP is involved in the regulation of platelet function and thrombosis.

– PFKP is one of the isoforms of phosphofructokinase-1 (PFK-1), 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, PFKP plays a crucial role in controlling the metabolic flux through this pathway, especially in proliferating cells that require higher energy and biosynthetic intermediates.

– Upregulated Expression: Many tumors demonstrate an increased expression of PFKP, which is consistent with the observed reliance on glycolysis (even in the presence of oxygen) for rapid energy production and biosynthesis.
– Metabolic Reprogramming: The overexpression of PFKP contributes to the enhanced glycolytic rate in cancer cells, supporting tumor growth, survival, and aggressiveness.
Scientific Papers found: Click to Expand⟱
1585- Citrate,    Sodium citrate targeting Ca2+/CAMKK2 pathway exhibits anti-tumor activity through inducing apoptosis and ferroptosis in ovarian cancer
- in-vitro, Ovarian, SKOV3 - in-vitro, Ovarian, A2780S - in-vitro, Nor, HEK293
Apoptosis↑,
Ferroptosis↑,
Ca+2↓, Sodium citrate chelates intracellular Ca2+
CaMKII ↓, inhibits the CAMKK2/AKT/mTOR/HIF1α-dependent glycolysis pathway, thereby inducing cell apoptosis.
Akt↓,
mTOR↓,
Hif1a↓,
ROS↑, Inactivation of CAMKK2/AMPK pathway reduces Ca2+ level in the mitochondria by inhibiting the activity of the MCU, resulting in excessive ROS production.
ChemoSen↑, Sodium citrate increases the sensitivity of ovarian cancer cells to chemo-drugs
Casp3↑,
Casp9↑,
BAX↑,
Bcl-2↓,
Cyt‑c↑, co-localization of cytochrome c and Apaf-1
GlucoseCon↓, glucose consumption, lactate production and pyruvate content were significantly reduced
lactateProd↓,
Pyruv↓,
GLUT1↓, sodium citrate decreased both mRNA and protein expression levels of glycolysis-related proteins such as Glut1, HK2 and PFKP
HK2↓,
PFKP↓,
Glycolysis↓, sodium citrate inhibited glycolysis of SKOV3 and A2780 cells
Hif1a↓, HIF1α expression was decreased significantly after sodium citrate treatment
p‑Akt↓, phosphorylation of AKT and mTOR was notably suppressed after sodium citrate treatment.
p‑mTOR↓,
Iron↑, ovarian cancer cells treated with sodium citrate exhibited higher Fe2+ levels, LPO levels, MDA levels, ROS and mitochondrial H2O2 levels
lipid-P↑,
MDA↑,
ROS↑,
H2O2↑,
mtDam↑, shrunken mitochondria, an increase in mitochondrial membrane density and disruption of mitochondrial cristae
GSH↓, (GSH) levels, GPX activity and expression levels of GPX4 were significantly reduced in SKOV3 and A2780 cells with sodium citrate treatment
GPx↓,
GPx4↓,
NADPH/NADP+↓, significant elevation in the NADP+/NADPH ratio was observed with sodium citrate treatment
eff↓, Fer-1, NAC and NADPH significantly restored the cell viability inhibited by sodium citrate
FTH1↓, decreased expression of FTH1
LC3‑Ⅱ/LC3‑Ⅰ↑, sodium citrate increased the conversion of cytosolic LC3 (LC3-I) to the lipidated form of LC3 (LC3-II)
NCOA4↑, higher levels of NCOA4
eff↓, test whether Ca2+ supplementation could rescue sodium citrate-induced ferroptosis. The results showed that Ca2+ dramatically reversed the enhanced levels of MDA, LPO and ROS triggered by sodium citrate
TumCG↓, sodium citrate inhibited tumor growth by chelation of Ca2+ in vivo

933- CUR,  EP,    Effective electrochemotherapy with curcumin in MDA-MB-231-human, triple negative breast cancer cells: A global proteomics study
- in-vitro, BC, NA
Apoptosis↑,
ALDOA↓,
ENO2↓,
LDHA↓, LDH inhibitor
LDHB↓,
PFKP↓,
PGK1↓,
PGM1↓,
PGAM1↓,
OXPHOS↑, upregulation of 10 oxidative phosphorylation pathway proteins
TCA↑, upregulation of 8 tricarboxylic acid (TCA) cycle proteins

2309- EGCG,  Chemo,    Targeting Glycolysis with Epigallocatechin-3-Gallate Enhances the Efficacy of Chemotherapeutics in Pancreatic Cancer Cells and Xenografts
- in-vitro, PC, MIA PaCa-2 - in-vitro, Nor, HPNE - in-vitro, PC, PANC1 - in-vivo, NA, NA
TumCG↓, EGCG reduced pancreatic cancer cell growth in a concentration-dependent manner
eff↑, and the growth inhibition effect was further enhanced under glucose deprivation conditions.
ROS↑, EGCG at 40 µM increased ROS levels by 1.4- and 1.6-fold in Panc-1 and MIA PaCa-2 cells, respectively
ECAR↓, EGCG affected glycolysis by suppressing the extracellular acidification rate through the reduction of the activity and levels of the glycolytic enzymes phosphofructokinase and pyruvate kinase.
ChemoSen↑, EGCG sensitized gemcitabine to inhibit pancreatic cancer cell growth in vitro and in vivo.
selectivity↑, EGCG at 80 µM for 72 h had significantly less effect on the HPNE cells, reducing cell growth by only 24%
Glycolysis↓, EGCG Inhibits Glycolysis through Suppressing Rate-Limiting Enzymes. EGCG Plus Gemcitabine Further Inhibits Glycolysis
PFK↓, EGCG treatment reduced both the activity and expression levels of phosphofructokinase (PFK) and pyruvate kinase (PK) in Panc-1 and MIA PaCa-2 cells
PKA↓,
HK2∅, EGCG failed to reduce hexokinases II (HK2) and lactate dehydrogenase A (LDHA) protein expression levels
LDHA∅,
PFKP↓, EGCG reduced the levels of PFKP and PKM2 (p < 0.01 for both) in pancreatic tumor xenograft homogenates, obtained from mice treated with EGCG
PKM2↓,
H2O2↑, EGCG at 40 µM increased H2O2 levels by 1.5- and 1.9-fold in Panc-1 and MIA PaCa-2 cells
TumW↓, EGCG and gemcitabine, given as single agents, reduced tumor weight by 40% and 52%, respectively, compared to vehicle-treated controls (p < 0.05 and p < 0.01). In combination, EGCG plus gemcitabine reduced tumor weight by 67%,

2344- QC,    Quercetin: A natural solution with the potential to combat liver fibrosis
- Review, Nor, NA
*HK2↓, By reducing the activity of key glycolytic enzymes—including hexokinase II (HK2), phosphofructokinase platelet (PFKP), and pyruvate kinase M2 (PKM2)—quercetin lowers energy production in LSECs, potentially slowing fibrosis progression.
*PFKP↓,
*PKM2↓,
*hepatoP↑, Quercetin lowered levels of liver enzymes (ALT, AST) and total bile acid, markers of liver injury.
*ALAT↓,
*AST↓,
*Glycolysis↓, quercetin inhibited glycolysis in LSECs, reducing lactate production, glucose consumption, and the expression of glycolytic enzymes
*lactateProd↓,
*GlucoseCon↓,
*CXCL1↓, By suppressing CXCL1 secretion, quercetin decreased neutrophil infiltration, a key factor in liver fibrosis, thereby effecting inflammation control.
*Inflam↓,

2410- SIL,    Autophagy activated by silibinin contributes to glioma cell death via induction of oxidative stress-mediated BNIP3-dependent nuclear translocation of AIF
- in-vitro, GBM, U87MG - in-vitro, GBM, U251 - in-vivo, NA, NA
TumAuto↑, Mechanistically, silibinin activates autophagy through depleting ATP by suppressing glycolysis.
ATP↓,
Glycolysis↓, Silibinin suppressed glycolysis in glioma cells
H2O2↑, Then, autophagy improves intracellular H2O2 via promoting p53-mediated depletion of GSH and cysteine and downregulation of xCT
P53↑,
GSH↓,
xCT↓,
BNIP3↝, The increased H2O2 promotes silibinin-induced BNIP3 upregulation and translocation to mitochondria
MMP↑, silibinin-induced mitochondrial depolarization, accumulation of mitochondrial superoxide
mt-ROS↑,
mtDam↑, Autophagy contributed to silibinin-induced mitochondria damage
HK2↓, protein levels of HK II, PFKP, and PKM2 were all downregulated time-dependently by silibinin in U87, U251, SHG-44, and C6 glioma cells
PFKP↓,
PKM2↓, silibinin suppressed glycolysis via downregulation of HK II, PFKP, and PKM2.
TumCG↓, Silibinin inhibited glioma cell growth in vivo


Showing Research Papers: 1 to 5 of 5

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

Ferroptosis↑, 1,   GPx↓, 1,   GPx4↓, 1,   GSH↓, 2,   H2O2↑, 3,   Iron↑, 1,   lipid-P↑, 1,   MDA↑, 1,   NADPH/NADP+↓, 1,   OXPHOS↑, 1,   ROS↑, 3,   mt-ROS↑, 1,   xCT↓, 1,  

Metal & Cofactor Biology ⓘ

FTH1↓, 1,   NCOA4↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↓, 1,   MMP↑, 1,   mtDam↑, 2,  

Core Metabolism/Glycolysis ⓘ

ALDOA↓, 1,   ECAR↓, 1,   ENO2↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 3,   HK2↓, 2,   HK2∅, 1,   lactateProd↓, 1,   LDHA↓, 1,   LDHA∅, 1,   LDHB↓, 1,   PFK↓, 1,   PFKP↓, 4,   PGAM1↓, 1,   PGK1↓, 1,   PGM1↓, 1,   PKM2↓, 2,   Pyruv↓, 1,   TCA↑, 1,  

Cell Death ⓘ

Akt↓, 1,   p‑Akt↓, 1,   Apoptosis↑, 2,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   Cyt‑c↑, 1,   Ferroptosis↑, 1,  

Kinase & Signal Transduction ⓘ

CaMKII ↓, 1,  

Autophagy & Lysosomes ⓘ

BNIP3↝, 1,   LC3‑Ⅱ/LC3‑Ⅰ↑, 1,   TumAuto↑, 1,  

DNA Damage & Repair ⓘ

P53↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

mTOR↓, 1,   p‑mTOR↓, 1,   TumCG↓, 3,  

Migration ⓘ

Ca+2↓, 1,   PKA↓, 1,  

Angiogenesis & Vasculature ⓘ

Hif1a↓, 2,  

Barriers & Transport ⓘ

GLUT1↓, 1,  

Drug Metabolism & Resistance ⓘ

ChemoSen↑, 2,   eff↓, 2,   eff↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

TumW↓, 1,  
Total Targets: 63

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

ALAT↓, 1,   GlucoseCon↓, 1,   Glycolysis↓, 1,   HK2↓, 1,   lactateProd↓, 1,   PFKP↓, 1,   PKM2↓, 1,  

Immune & Inflammatory Signaling ⓘ

CXCL1↓, 1,   Inflam↓, 1,  

Clinical Biomarkers ⓘ

ALAT↓, 1,   AST↓, 1,  

Functional Outcomes ⓘ

hepatoP↑, 1,  
Total Targets: 12

Scientific Paper Hit Count for: PFKP, Phosphofructokinase, Platelet
1 Citric Acid
1 Curcumin
1 Electrical Pulses
1 EGCG (Epigallocatechin Gallate)
1 Chemotherapy
1 Quercetin
1 Silymarin (Milk Thistle) silibinin
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#:771  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page