CDC25 Cancer Research Results

CDC25, Cell Division Cycle 25: Click to Expand ⟱
Source:
Type:
CDC25 (Cell Division Cycle 25) is a family of dual-specificity phosphatases that play a crucial role in regulating the cell cycle. There are three main isoforms of CDC25: CDC25A, CDC25B, and CDC25C. These proteins are involved in the activation of cyclin-dependent kinases (CDKs) by dephosphorylating them, which is essential for the progression of the cell cycle from G2 phase to mitosis.
CDC25 proteins, particularly CDC25A, are often found to be overexpressed in various types of cancer. This overexpression can lead to uncontrolled cell proliferation, as the normal regulatory mechanisms of the cell cycle are disrupted.
High levels of CDC25 have been associated with advanced stages of cancer and poor prognosis in several malignancies, including breast, colorectal, and prostate cancers.
CDC25 interacts with various oncogenes and tumor suppressor proteins, such as p53. The loss of p53 function, which is common in many cancers, can lead to increased CDC25 activity, further promoting tumorigenesis.
CDC25A overexpressed: breast, CRC, lung, prostate.
CDC25B: breast, ovarian, lung.
CDC25C: liver,breast, prostate.
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: CDC25, Cell Division Cycle 25
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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