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隐秘的lncRNA编码的微蛋白TPM3P9驱动瘤性RNA剪接和瘤发生

Kun Meng^1,2, Yuying Li¹, Xiaoyi Yuan¹

¹MOE Key Laboratory of Tumor Molecular Biology and State Key Laboratory of Bioactive Molecules and Druggability Assessment, Institute of Life and Health Engineering, College of Life Science and Technology, Jinan University, Guangzhou, 510632, China.

Signal transduction and targeted therapy

|January 26, 2025

概括

一种来自非编码RNA的新型微蛋白TPM3P9通过改变RNA拼接来驱动清细胞细胞癌 (ccRCC) 的进展. 这一发现为癌提供了新的预后和治疗标.

科学领域:

分子瘤学分子瘤学
在RNA生物学,RNA生物学.
癌症基因组学癌症基因组学

背景情况:

非编码RNA可以产生具有致癌潜力的微蛋白质.
微蛋白在替代拼接驱动的瘤进展中的作用在很大程度上尚未被探索.

研究的目的:

研究微蛋白TPM3P9在清细胞细胞癌 (ccRCC) 中的功能和机制.
探索TPM3P9在替代拼接中的作用及其在ccRCC中的临床意义.

主要方法:

鉴定出TPM3P9是一种微蛋白,由lncRNA-tropomyosin 3假基因9编码.
研究了TPM3P9与拼接因子RBM4的相互作用及其对TCF7L2拼接的影响.
分析了ccRCC组织中的TPM3P9表达,并将其与临床结果相关联.

主要成果:

TPM3P9的过度表达促进了ccRCC细胞的增殖和瘤的生长.
在TCF7L2中,TPM3P9抑制了RBM4介导的外因子跳转,增加了致癌的TCF7L2-L变异体.
TPM3P9对NF-κB信号通路组件RELB进行上调.
TPM3P9表达与TCF7L2-L和RELB水平相关,并预测患者的生存率较低.

结论:

非编码RNA衍生的微蛋白TPM3P9通过调节RNA拼接,在ccRCC中具有致癌性.
TPM3P9,RBM4,TCF7L2-L和RELB代表癌的潜在预后和治疗标.

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