CHK1 Cancer Research Results

CHK1, Checkpoint Kinase 1: Click to Expand ⟱
Source:
Type:
A protein that plays a crucial role in the DNA damage response pathway. It is involved in the repair of DNA damage and the maintenance of genome stability.
CHK1 acts as a tumor suppressor by preventing the accumulation of DNA damage and maintaining genome stability. Loss of CHK1 function can lead to increased genetic instability and a higher risk of cancer.
-CHK1 is often overexpressed in various types of cancer, including breast, colorectal, lung, and ovarian cancer. Overexpression of CHK1 can contribute to the development of resistance to chemotherapy and radiation therapy.
-CHK1 expression is often higher in tumor cells compared to normal cells. This tumor-specific expression makes CHK1 a potential target for cancer therapy.
Scientific Papers found: Click to Expand⟱
6976- Form,    Study on the Mechanism of Formononetin Against Hepatocellular Carcinoma: Regulating Metabolic Pathways of Ferroptosis and Cell Cycle
- vitro+vivo, HCC, HepG2
ROS↑, results showed that FM induces oxidative DNA damage through ROS generation and triggers G2/M phase cell cycle arrest via the Chk1/Cdc25C/CDK1/CCNB1 signaling pathway.
DNAdam↑,
TumCCA↑,
CHK1↝,
CDC25↝,
CDK1↝,
CycB/CCNB1↝,
GSH↓, FM limited the synthesis of glutathione, promoted lipid peroxidation, and facilitated the generation of divalent iron.
lipid-P↑,
Ferroptosis↑, FM induces ferroptosis by inhibiting the p53/xCT/GPX4 signaling pathway.
xCT↓,
P53↓,
GPx4↓,
other↝, FM could induce DNA damage leading to cell cycle arrest and may also induce ferroptosis by regulating glutathione metabolism, thereby intervening in the occurrence and development of HCC
TumCP↓, FM Inhibits the Proliferation of HepG2 Cells
γH2AX↑, results revealed a significant down-expression of H2A.X and an up-expression of γ-H2A.X,
TumCG↓, FM Inhibits Tumor Growth In Vivo
Ki-67↓, FM could downregulate the expression of proliferation markers Ki67 and PCNA, as well as the ferroptosis marker GPX4
PCNA↓,
MMP↓, FM could induce the accumulation of ROS and a decrease in MMP in HepG2 cells in a dose-dependent manner


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(tgid=1) ⓘ

Ferroptosis↑, 1,   GPx4↓, 1,   GSH↓, 1,   lipid-P↑, 1,   ROS↑, 1,   xCT↓, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

CDC25↝, 1,   MMP↓, 1,  

Cell Death(tgid=5) ⓘ

Ferroptosis↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↝, 1,  

DNA Damage & Repair(tgid=10) ⓘ

CHK1↝, 1,   DNAdam↑, 1,   P53↓, 1,   PCNA↓, 1,   γH2AX↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK1↝, 1,   CycB/CCNB1↝, 1,   TumCCA↑, 1,  

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

TumCG↓, 1,  

Migration(tgid=13) ⓘ

Ki-67↓, 1,   TumCP↓, 1,  

Clinical Biomarkers(tgid=22) ⓘ

Ki-67↓, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: CHK1, Checkpoint Kinase 1
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

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