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NELFCD Promotes Colon Cancer Progression by Regulating the DUSP2-p38 Axis
Weiwei Dai1, Min Zhu1, Yujing Sun2
1Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, State Key Laboratory of Digestive Health, National Clinical Research Center for Digestive Diseases, 100000, Beijing, China.
Frontiers in Bioscience (Landmark Edition)
|April 30, 2025
Summary
The negative elongation factor complex member C/D (NELFCD) promotes colon cancer growth by inhibiting DUSP2 expression via PRMT5 recruitment. Targeting this NELFCD-DUSP2-p38 pathway offers a potential therapeutic strategy for colon cancer.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Genetics
Background:
- Colon cancer progression is a significant health concern.
- The role of the negative elongation factor complex member C/D (NELFCD) in colon cancer remains largely unexplored.
Purpose of the Study:
- To investigate the role and mechanism of NELFCD in colon cancer progression.
- To identify potential therapeutic targets within the NELFCD signaling pathway.
Main Methods:
- Utilized immunohistochemistry, Western blot, and RT-qPCR to assess NELFCD and DUSP2 expression.
- Employed co-immunoprecipitation and chromatin immunoprecipitation assays to determine molecular interactions.
- Assessed cell proliferation and cell cycle progression using cell counting kit-8, colony formation, and flow cytometry.
Main Results:
- NELFCD expression is upregulated in colon cancer and correlates with increased cancer cell growth.
- NELFCD negatively regulates DUSP2 expression and directly targets DUSP2 and MAPK pathway genes.
- NELFCD interacts with PRMT5, promoting PRMT5 enrichment at the DUSP2 promoter.
Conclusions:
- NELFCD promotes colon cancer progression by recruiting PRMT5 to suppress DUSP2, thereby activating the p38 signaling pathway.
- The NELFCD-DUSP2-p38 signaling axis represents a potential therapeutic target for NELFCD-amplified colon tumors.
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