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Published on: May 14, 2016
IL-24 Induces Cell Dormancy and Oxaliplatin Resistance in Colon Cancer Cells by Activating NF-κB Pathway
Yanyan Hu1, Shengying Li2, Minjing Zhu1
1Clinical Laboratory, Sanmen People's Hospital, Sanmen, China.
Molecular Carcinogenesis
|July 16, 2026
Summary
Interleukin-24 (IL-24) promotes colon cancer cell dormancy and oxaliplatin resistance by activating the NF-κB pathway. Targeting the IL-24/NF-κB axis may overcome chemotherapy resistance in colon cancer patients.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Oxaliplatin is a key treatment for colon cancer, but drug resistance limits its effectiveness.
- Cancer cell dormancy is a known contributor to chemotherapy resistance.
- The role of Interleukin-24 (IL-24) in colon cancer dormancy and oxaliplatin resistance was previously unexplored.
Purpose of the Study:
- To investigate the function of IL-24 in colon cancer cell dormancy and resistance to oxaliplatin.
- To elucidate the underlying molecular mechanism of IL-24's action in colon cancer.
Main Methods:
- Assessed IL-24 expression in colon cancer tissues and cells using RT-qPCR, western blotting, and immunohistochemistry.
- Evaluated IL-24's effects on cell proliferation, apoptosis, dormancy, and oxaliplatin resistance via CCK-8 assays, flow cytometry, and western blotting.
- Utilized RNA sequencing, bioinformatics analyses, and a tumor xenograft mouse model to explore the IL-24 downstream mechanism involving the NF-κB pathway.
Main Results:
- IL-24 was found to be overexpressed in oxaliplatin-resistant colon cancer tissues and cells.
- IL-24 treatment promoted colon cancer cell dormancy by inducing G0/G1 cell cycle arrest and upregulating dormancy markers.
- IL-24 activated the NF-κB signaling pathway, and inhibiting NF-κB reversed IL-24-induced dormancy and oxaliplatin resistance.
- In vivo studies confirmed that IL-24 promotes tumor dormancy and oxaliplatin resistance by activating NF-κB signaling.
Conclusions:
- IL-24 induces colon cancer cell dormancy and oxaliplatin resistance through the activation of NF-κB signaling.
- The IL-24/NF-κB axis represents a potential therapeutic target for overcoming oxaliplatin resistance in colon cancer.
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