RNA-binding protein RALYL-mediated BCL11B RNA stability promotes immune escape in small cell lung cancer through transcriptional activation of BUB3.

Jiayue Shao, Shuangqing Liu, Ling Qin, Ningning Fan, Qi Sun, Qingwei Meng

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Article in Cellular oncology (Dordrecht, Netherlands), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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6 authors.

Jiayue ShaoDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Harbin, Heilongjiang, 150081, P.R. China.

Shuangqing LiuDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Harbin, Heilongjiang, 150081, P.R. China.

Ling QinDepartment of Pathology, Harbin Medical University Cancer Hospital, Harbin, Heilongjiang, 150081, P.R. China.

Ningning FanDepartment of Clinical Laboratory, the First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, P.R. China.

Qi SunDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Harbin, Heilongjiang, 150081, P.R. China.

Qingwei MengDepartment of Medical Oncology, Harbin Medical University Cancer Hospital, No. 150, Haping Road, Harbin, Heilongjiang, 150081, P.R. China. mengqw@hrbmu.edu.cn.ORCID https://orcid.org/0000-0002-7388-8181

Funding

the Key Research and Development Program of Heilongjiang 2022ZX06C11the Nn10 Program of Harbin Medical University Cancer Hospital Nn10pv2017-04

6 · The paper itself

Abstract

purposeSmall 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.

methodsClinical 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.

resultsBCL11B was notably increased in SCLC tissues and was associated with poor prognoses. BCL11B knockdown repressed SCLC cells from CD8

conclusionRALYL increases BCL11B stability and activates BUB3 to induce immune escape in SCLC by enhancing PD-L1 expression.

Indexed as

Cell Cycle ProteinsLung NeoplasmsProtein Serine-Threonine KinasesRepressor ProteinsRNA-Binding ProteinsRNA StabilitySmall Cell Lung CarcinomaTranscriptional ActivationTumor EscapeTumor Suppressor ProteinsAnimalsCD8-Positive T-LymphocytesCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansBCL11B protein, humanBUB3 protein, humanCell Cycle ProteinsPoly-ADP-Ribose Binding ProteinsProtein Serine-Threonine KinasesRepressor ProteinsRNA-Binding ProteinsTumor Suppressor ProteinsBCL11BCD8+ T cellsEpigeneticsImmunotherapySmall cell lung cancer

Identifiers

PMID42455237

DOI10.1007/s13402-026-01261-y

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