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Published on: October 31, 2013
CELF2 inhibits bladder cancer progression by decreasing the stability of CXCL5
Shiqiang Dong1, Lili Wang2, Xinyu Liu3
1Department of Urology, Urologic Surgery Center, Xinqiao Hospital, Third Military Medical University (Army Medical University), Chongqing 400037, China; Department of Oncology, Second Hospital of Tianjin Medical University, Tianjin Institute of Urology, Tianjin Key Laboratory of Precision Medicine for Sex Hormones and Diseases, Tianjin 300211, China.
Aims:
CUGBP Elav-like family (CELF), an RNA-binding protein group, has been implicated in numerous diseases, including cancer. The role of CELF2 in bladder cancer is still not well understood. This study aims to investigate the role of CELF2 in bladder cancer in vitro and in vivo using bioinformatics, biochemical, and functional methods.
Materials And Methods:
We explored CELF2 and CELFs expression patterns and their association with bladder cancer by analyzing The Cancer Genome Atlas, University of California, Santa Cruz XENA, and Cancer Cell Line Encyclopedia databases using various computational and statistical analyses, including unsupervised clustering, Kaplan-Meier analysis, and correlation assessments. We utilized the bladder cancer cell lines T24 and J82 for functional analyses. We performed in vitro and in vivo experiments to investigate the impact of CELF2 expression levels on bladder cancer cell proliferation and migration.
Key Findings:
CELF2 expression was downregulated in bladder cancer and positively correlated with the progression-free interval in patients. Increased CELF2 expression suppressed the proliferation and migration of bladder cancer cells. Furthermore, CELF2 was bound to AU-rich motifs in the 3'-UTR of CXCL5, reducing its stability, inhibiting CXCL5/CXCR2/AKT signaling, and repressing bladder cancer progression. Finally, we developed a prognostic model that revealed CELF2 and CXCL5 as independent prognostic factors for progression-free intervals in patients with bladder cancer.
Significance:
CELF2 reduced the stability of CXCL5 and suppressed the proliferation and migration of bladder cancer cells by inhibiting p-AKT expression. The findings of this study highlight CELF2 as a potential therapeutic target for bladder cancer treatment.
Insights
CUGBP Elav-like family member 2 (CELF2) suppresses bladder cancer progression by reducing CXCL5 stability and inhibiting AKT signaling. This study identifies CELF2 as a potential therapeutic target for bladder cancer.
Area of Science:
- Oncology
- Molecular Biology
- Genomics
Background:
- CUGBP Elav-like family (CELF) proteins are RNA-binding proteins implicated in various diseases, including cancer.
- The specific role of CELF2 in bladder cancer remains largely uncharacterized.
- Understanding CELF2's function is crucial for developing novel bladder cancer therapies.
Purpose of the Study:
- To investigate the role of CELF2 in bladder cancer.
- To analyze CELF2 expression patterns and their correlation with patient outcomes.
- To elucidate the molecular mechanisms underlying CELF2's function in bladder cancer cells.
Main Methods:
- Bioinformatic analysis of The Cancer Genome Atlas, UCSC XENA, and CCLE databases.
- In vitro and in vivo functional assays using bladder cancer cell lines (T24, J82).
- Assessment of CELF2's impact on cell proliferation, migration, and target gene stability (CXCL5).
Main Results:
- CELF2 expression is downregulated in bladder cancer and correlates with improved progression-free survival.
- Overexpression of CELF2 suppresses bladder cancer cell proliferation and migration.
- CELF2 binds to CXCL5 mRNA, reducing its stability and inhibiting the CXCL5/CXCR2/AKT signaling pathway.
- CELF2 and CXCL5 are identified as independent prognostic factors for progression-free intervals.
Conclusions:
- CELF2 suppresses bladder cancer progression by destabilizing CXCL5 mRNA and inhibiting AKT signaling.
- CELF2 demonstrates potential as a therapeutic target for bladder cancer treatment.
- The study provides insights into the molecular mechanisms of CELF2 in bladder cancer.
