PDK1 / PDPK1 Cancer Research Results

PDK1 / PDPK1, Pyruvate dehydrogenase kinase 1: Click to Expand ⟱
Source:
Type:

PDPK1 - 3-Phosphoinositide-Dependent Protein Kinase 1

Abbreviation: PDPK1, PDK1

Type: Serine/threonine protein kinase / PI3K pathway signaling kinase / AGC kinase activator

Function: PDPK1 is a central signaling kinase downstream of phosphoinositide 3-kinase. It phosphorylates and activates multiple AGC-family kinases, including AKT, S6K, SGK, RSK, and selected PKC isoforms, thereby regulating proliferation, survival, metabolism, migration, and cellular growth.

Cancer: ↑ Frequently overexpressed, hyperactivated, or functionally dysregulated in cancer. Increased PDPK1 signaling enhances PI3K-AKT pathway output, proliferation, survival, migration, invasion, metastasis, metabolic adaptation, and resistance to anticancer therapies. Genetic or pharmacological suppression of PDPK1 can inhibit tumor growth and restore treatment sensitivity in experimental models.

Favorable Direction in Cancer: ↓ PDPK1 expression or kinase activity is generally favorable.
NA, Not Available: Click to Expand ⟱
none (reserved)
Scientific Papers found: Click to Expand⟱
943- BetA,    Betulinic acid suppresses breast cancer aerobic glycolysis via caveolin-1/NF-κB/c-Myc pathway
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231 - in-vivo, NA, NA
Glycolysis↓, lactateProd↓, GlucoseCon↓, ECAR↓, cMyc↓, LDHA↓, p‑PDK1 / PDPK1↓, PDK1 / PDPK1↓, Cav1↑, *Glycolysis↑, selectivity↑, OCR↓, OXPHOS↓,
2738- BetA,    Betulinic Acid Suppresses Breast Cancer Metastasis by Targeting GRP78-Mediated Glycolysis and ER Stress Apoptotic Pathway
- in-vitro, BC, MDA-MB-231 - in-vitro, BC, BT549 - in-vivo, NA, NA
TumCI↓, TumCMig↓, Glycolysis↓, lactateProd↓, GRP78/BiP↑, ER Stress↑, PERK↑, p‑eIF2α↑, β-catenin/ZEB1↓, cMyc↓, ROS↑, angioG↓, Sp1/3/4↓, DNAdam↑, TOP1↓, TumMeta↓, MMP2↓, MMP9↓, N-cadherin↓, Vim↓, E-cadherin↑, EMT↓, LDHA↓, p‑PDK1 / PDPK1↓, PDK1 / PDPK1↓, ECAR↓, OCR↓, Hif1a↓, STAT3↓,
1591- Citrate,    The biological significance of cancer: mitochondria as a cause of cancer and the inhibition of glycolysis with citrate as a cancer treatment
- Analysis, NA, NA
Glycolysis↓, PDK1 / PDPK1↓, SDH↓,
2044- PB,  DCA,    Differential inhibition of PDKs by phenylbutyrate and enhancement of pyruvate dehydrogenase complex activity by combination with dichloroacetate
- in-vivo, NA, NA
PDK1 / PDPK1↓, PDKs↓, eff↑, PDH↑,
998- PB,    Phenyl butyrate inhibits pyruvate dehydrogenase kinase 1 and contributes to its anti-cancer effect
- in-vivo, NA, NA
p‑PDH↓, PDH↑, PDK1 / PDPK1↓, HDAC↓, Glycolysis↓, MMP↓, Apoptosis↑,

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(tgid=1) ⓘ

OXPHOS↓, 1,   ROS↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

MMP↓, 1,   OCR↓, 2,   SDH↓, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Cav1↑, 1,   cMyc↓, 2,   ECAR↓, 2,   GlucoseCon↓, 1,   Glycolysis↓, 4,   lactateProd↓, 2,   LDHA↓, 2,   PDH↑, 2,   p‑PDH↓, 1,   PDK1 / PDPK1↓, 5,   p‑PDK1 / PDPK1↓, 2,   PDKs↓, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

Sp1/3/4↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

p‑eIF2α↑, 1,   ER Stress↑, 1,   GRP78/BiP↑, 1,   PERK↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

EMT↓, 1,   HDAC↓, 1,   STAT3↓, 1,   TOP1↓, 1,  

Migration(tgid=13) ⓘ

E-cadherin↑, 1,   MMP2↓, 1,   MMP9↓, 1,   N-cadherin↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumMeta↓, 1,   Vim↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

eff↑, 1,   selectivity↑, 1,  
Total Targets: 41

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↑, 1,  
Total Targets: 1

Scientific Paper Hit Count for: PDK1 / PDPK1, Pyruvate dehydrogenase kinase 1
2 Betulinic acid
2 Phenylbutyrate
1 Citric Acid
1 Dichloroacetate
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:0  Cells:%  prod#:%  Target#:246  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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