PCK1 Cancer Research Results

PCK1, phosphoenolpyruvate carboxykinase 1: Click to Expand ⟱
Source:
Type:
Compelling evidence suggests that PCK1 is strongly expressed in CRC cells and that PCK1 promotes cancer cell proliferation by increasing the anabolic utilization of glucose and glutamine. The expression of PCK1 in cancer is tissue-specific.

PCK1’s expression and role in cancer are complex and vary by tissue type and tumor microenvironment. In cancers such as hepatocellular carcinoma, PCK1 is often downregulated and this reduction is associated with poorer prognosis and a more aggressive tumor phenotype, suggesting a tumor-suppressive role. In other cancers such as colorectal, lung, or breast cancer, findings are mixed and depend on the metabolic context, with some evidence pointing to altered PCK1 levels contributing to metabolic reprogramming that supports tumor growth.


Scientific Papers found: Click to Expand⟱
1184- DHA,    Syndecan-1-Dependent Suppression of PDK1/Akt/Bad Signaling by Docosahexaenoic Acid Induces Apoptosis in Prostate Cancer
- in-vitro, Pca, PC3 - in-vitro, Pca, LNCaP - in-vivo, NA, NA
SDC1↑,
p‑PCK1↓,
Akt↓,
BAD↓,

2827- FIS,    The Potential Role of Fisetin, a Flavonoid in Cancer Prevention and Treatment
- Review, Var, NA
*antiOx↑, effective antioxidant, anti-inflammatory
*Inflam↓,
neuroP↑, neuro-protective, anti-diabetic, hepato-protective and reno-protective potential.
hepatoP↑,
RenoP↑,
cycD1/CCND1↓, Figure 3
TumCCA↑,
MMPs↓,
VEGF↓,
MAPK↓,
NF-kB↓,
angioG↓,
Beclin-1↑,
LC3s↑,
ATG5↑,
Bcl-2↓,
BAX↑,
Casp↑,
TNF-α↓,
Half-Life↓, Fisetin was given at an effective dosage of 223 mg/kilogram intraperitoneally in mice. The plasma concentration declined biophysically, with a rapid half-life of 0.09 h and a terminal half-life of 3.1 h,
MMP↓, Fisetin powerfully improved apoptotic cells and caused the depolarization of the mitochondrial membrane.
mt-ROS↑, Fisetin played a role in the induction of apoptosis, independently of p53, and increased mitochondrial ROS generation.
cl‑PARP↑, fisetin-induced sub-G1 population as well as PARP cleavage.
CDK2↓, Moreover, the activities of cyclin-dependent kinases (CDK) 2 as well as CDK4 were decreased by fisetin and also inhibited CDK4 activity in a cell-free system, demonstrating that it might directly inhibit the activity of CDK4
CDK4↓,
Cyt‑c↑, Moreover, release of cytochrome c and Smac/Diablo was induced by fisetin
Diablo↑,
DR5↑, Fisetin caused an increase in the protein levels of cleaved caspase-8, DR5, Fas ligand, and TNF-related apoptosis-inducing ligand
Fas↑,
PCNA↓, Fisetin decreased proliferation-related proteins such as PCNA, Ki67 and phosphorylated histone H3 (p-H3) and decreased the expression of cell growth
Ki-67↓,
p‑H3↓,
chemoP↑, Paclitaxel treatment only showed more toxicity to normal cells than the combination of flavonoids with paclitaxel, suggesting that fisetin might bring some safety against paclitaxel-facilitated cytotoxicity.
Ca+2↑, Fisetin encouraged apoptotic cell death via increased ROS and Ca2+, while it increased caspase-8, -9 and -3 activities and reduced the mitochondrial membrane potential in HSC3 cells.
Dose↝, After fisetin treatment at 40 µM, invasion was reduced by 87.2% and 92.4%, whereas after fisetin treatment at 20 µM, invasion was decreased by 52.4% and 59.4% in SiHa and CaSki cells, respectively
CDC25↓, This study proposes that fisetin caused the arrest of the G2/M cell cycle via deactivating Cdc25c as well Cdc2 via the activation of Chk1, 2 and ATM
CDC2↓,
CHK1↑,
Chk2↑,
ATM↑,
PCK1↓, fisetin decreases the levels of SOS-1, pEGFR, GRB2, PKC, Ras, p-p-38, p-ERK1/2, p-JNK, VEGF, FAK, PI3K, RhoA, p-AKT, uPA, NF-ĸB, MMP-7,-9 and -13, whereas it increases GSK3β as well as E-cadherin in U-2 OS
RAS↓,
p‑p38↓,
Rho↓,
uPA↓,
MMP7↓,
MMP13↓,
GSK‐3β↑,
E-cadherin↑,
survivin↓, whereas those of survivin and BCL-2 were reduced in T98G cells
VEGFR2↓, Fisetin inhibited the VEGFR expression in Y79 cells as well as the angiogenesis of a tumor.
IAP2↓, The downregulation of cIAP-2 by fisetin
STAT3↓, fisetin induced apoptosis in TPC-1 cells via the initiation of oxidative damage and enhanced caspases expression by downregulating STAT3 and JAK 1 signaling
JAK1↓,
mTORC1↓, Fisetin acts as a dual inhibitor of mTORC1/2 signaling,
mTORC2↓,
NRF2↑, Moreover, In JC cells, the Nrf2 expression was gradually increased by fisetin from 8 h to 24 h

193- MFrot,  MF,    Rotating Magnetic Field Mitigates Ankylosing Spondylitis Targeting Osteocytes and Chondrocytes via Ameliorating Immune Dysfunctions
- in-vivo, Arthritis, NA
BMD↑, loss reduced
Cartilage↑, more intact cartilage surfaces and denser proteoglycan
IL17↓,
IL22↓,
IL23↓,
IL28↓,
CD4+↓, tremendously attenuated
CD8+↓, In this investigation, data showed that RMF treatment decreased CD3-expressing proliferative cells via immunostaining and reduced CD4+/CD8+ T-cells via flow cytometry in AS mice
LAMB3↑,
COL4↓,
THBS2↓,
ITGA11↓,
PPARγ↑, mice have decreased expression of peroxisome proliferator-activated receptor γ (PPAR-γ), a ligand-activated transcription factor belonging to the nuclear hormone receptor superfamily, which RMF reverses.
ACAA1↓,
PLIN1↓,
FABP4↓,
PCK1↓,
UCP1↓,
TNF-α↓,


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 ⓘ

NRF2↑, 1,   mt-ROS↑, 1,  

Mitochondria & Bioenergetics ⓘ

CDC2↓, 1,   CDC25↓, 1,   MMP↓, 1,   UCP1↓, 1,  

Core Metabolism/Glycolysis ⓘ

ACAA1↓, 1,   FABP4↓, 1,   PCK1↓, 2,   p‑PCK1↓, 1,   PLIN1↓, 1,   PPARγ↑, 1,  

Cell Death ⓘ

Akt↓, 1,   BAD↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp↑, 1,   Chk2↑, 1,   Cyt‑c↑, 1,   Diablo↑, 1,   DR5↑, 1,   Fas↑, 1,   IAP2↓, 1,   MAPK↓, 1,   p‑p38↓, 1,   survivin↓, 1,  

Transcription & Epigenetics ⓘ

p‑H3↓, 1,  

Autophagy & Lysosomes ⓘ

ATG5↑, 1,   Beclin-1↑, 1,   LC3s↑, 1,  

DNA Damage & Repair ⓘ

ATM↑, 1,   CHK1↑, 1,   cl‑PARP↑, 1,   PCNA↓, 1,  

Cell Cycle & Senescence ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↑, 1,   mTORC1↓, 1,   mTORC2↓, 1,   RAS↓, 1,   STAT3↓, 1,  

Migration ⓘ

Ca+2↑, 1,   Cartilage↑, 1,   COL4↓, 1,   E-cadherin↑, 1,   ITGA11↓, 1,   Ki-67↓, 1,   LAMB3↑, 1,   MMP13↓, 1,   MMP7↓, 1,   MMPs↓, 1,   Rho↓, 1,   SDC1↑, 1,   THBS2↓, 1,   uPA↓, 1,  

Angiogenesis & Vasculature ⓘ

angioG↓, 1,   VEGF↓, 1,   VEGFR2↓, 1,  

Immune & Inflammatory Signaling ⓘ

CD4+↓, 1,   IL17↓, 1,   IL22↓, 1,   IL23↓, 1,   IL28↓, 1,   JAK1↓, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance ⓘ

Dose↝, 1,   Half-Life↓, 1,  

Clinical Biomarkers ⓘ

BMD↑, 1,   Ki-67↓, 1,  

Functional Outcomes ⓘ

chemoP↑, 1,   hepatoP↑, 1,   neuroP↑, 1,   RenoP↑, 1,  

Infection & Microbiome ⓘ

CD8+↓, 1,  
Total Targets: 77

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  
Total Targets: 2

Scientific Paper Hit Count for: PCK1, phosphoenolpyruvate carboxykinase 1
1 Docosahexaenoic Acid
1 Fisetin
1 Magnetic Field Rotating
1 Magnetic Fields
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#:552  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

 

Home Page