Life sciences · 2025
CELF2 inhibits bladder cancer progression by decreasing the stability of CXCL5.
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Dong Shiqiang, Wang Lili, Liu Xinyu, Hou Dingkun, Liu Qing, Zheng Ji, Wang Haitao
Аннотация
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.
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.