Cellular oncology (Dordrecht, Netherlands) · 2026
RNA-binding protein RALYL-mediated BCL11B RNA stability promotes immune escape in small cell lung cancer through transcriptional activation of BUB3.
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Shao Jiayue, Liu Shuangqing, Qin Ling, Fan Ningning, Sun Qi, Meng Qingwei
Аннотация
PURPOSE: Small cell lung cancer (SCLC) is marked by rapid tumor growth and poor outcomes and necessitates effective treatments. This paper explores the molecular mechanisms by which BCL11B affects immune escape in SCLC.
METHODS: Clinical tissues were collected to analyze BCL11B expression in SCLC, and the correlations between BCL11B and prognosis were examined. A co-culture system of SCLC and T cells was constructed to analyze immune escape. A transplanted tumor model was constructed, and the efficacy of PD-L1 immunotherapy was analyzed after BCL11B knockdown. The downstream targets of BCL11B were screened by bioinformatics, and BUB3 expression was verified in clinical tissues. The regulation of BCL11B on BUB3 was examined. Rescue assays were designed to analyze immune escape and tumor immunotherapy after BUB3 overexpression. RNA-binding proteins that regulated BCL11B were predicted, and their expression and prognostic significance in SCLC were analyzed. The effect of RALYL on immune escape was validated in vitro.
RESULTS: BCL11B was notably increased in SCLC tissues and was associated with poor prognoses. BCL11B knockdown repressed SCLC cells from CD8+ T-mediated cytotoxicity, enhanced the efficacy of PD-L1 immunotherapy, and blocked SCLC progression. BCL11B transcriptionally activated BUB3 and enhanced PD-L1 expression. BUB3 overexpression reversed the impact of BCL11B knockdown on immune escape and the efficacy of immunotherapy. RALYL increased BCL11B mRNA stability to activate BUB3 and enhance PD-L1 expression. RALYL knockdown prevented immune escape in SCLC cells.
CONCLUSION: RALYL increases BCL11B stability and activates BUB3 to induce immune escape in SCLC by enhancing PD-L1 expression.
METHODS: Clinical tissues were collected to analyze BCL11B expression in SCLC, and the correlations between BCL11B and prognosis were examined. A co-culture system of SCLC and T cells was constructed to analyze immune escape. A transplanted tumor model was constructed, and the efficacy of PD-L1 immunotherapy was analyzed after BCL11B knockdown. The downstream targets of BCL11B were screened by bioinformatics, and BUB3 expression was verified in clinical tissues. The regulation of BCL11B on BUB3 was examined. Rescue assays were designed to analyze immune escape and tumor immunotherapy after BUB3 overexpression. RNA-binding proteins that regulated BCL11B were predicted, and their expression and prognostic significance in SCLC were analyzed. The effect of RALYL on immune escape was validated in vitro.
RESULTS: BCL11B was notably increased in SCLC tissues and was associated with poor prognoses. BCL11B knockdown repressed SCLC cells from CD8+ T-mediated cytotoxicity, enhanced the efficacy of PD-L1 immunotherapy, and blocked SCLC progression. BCL11B transcriptionally activated BUB3 and enhanced PD-L1 expression. BUB3 overexpression reversed the impact of BCL11B knockdown on immune escape and the efficacy of immunotherapy. RALYL increased BCL11B mRNA stability to activate BUB3 and enhance PD-L1 expression. RALYL knockdown prevented immune escape in SCLC cells.
CONCLUSION: RALYL increases BCL11B stability and activates BUB3 to induce immune escape in SCLC by enhancing PD-L1 expression.