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Updated: May 4, 2026
12:02
Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
Published on: June 6, 2017
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Interleukin-17F attenuates H2O2-induced cell cycle arrest
Zan Tong1, Huichao Yan2, Weihuang Liu1
1School of Basic Medical Sciences, Wuhan University, Wuhan 430071, China.
Cellular Immunology
|January 16, 2014
Summary
Interleukin (IL)-17F plays a role in colon cancer by preventing cell cycle arrest. This study shows IL-17F inhibits oxidant-induced G2/M phase arrest in colon cancer cells, impacting cell cycle regulators.
Area of Science:
- Oncology
- Cell Biology
- Molecular Biology
Background:
- Interleukin (IL)-17F is present in colon epithelial cells and influences colon tumorigenesis.
- The specific role of IL-17F in colon cancer cell cycle progression is not well understood.
Purpose of the Study:
- To investigate the effect of IL-17F on oxidant-induced cell cycle changes in human colon cancer cells.
- To elucidate the molecular mechanisms by which IL-17F influences cell cycle regulation.
Main Methods:
- Utilized IL-17F overexpressing and wildtype HCT116 cells.
- Applied hydrogen peroxide (H2O2) to challenge cells.
- Performed cell cycle distribution analysis.
- Assessed expression levels of p21 and p27.
- Measured p38 phosphorylation.
Main Results:
- IL-17F attenuated H2O2-induced G2/M phase arrest by inhibiting the S to G2/M transition.
- IL-17F suppressed H2O2-induced upregulation of the cell cycle regulator p27.
- IL-17F increased p38 phosphorylation following H2O2 treatment.
Conclusions:
- IL-17F influences colon cancer cell cycle progression by modulating p27 levels and p38 activity.
- These regulatory effects contribute to impaired G2/M phase arrest.
- IL-17F is identified as a significant factor in colon cancer development, offering new insights into its signaling pathway.
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