涉及剪接因子SRRM1的b细胞急性淋巴细胞白血病的会聚性恶性表型。

NAR Cancer Pub Date : 2022-12-01 DOI:10.1093/narcan/zcac041
Adria Closa, Marina Reixachs-Solé, Antonio C Fuentes-Fayos, Katharina E Hayer, Juan L Melero, Fabienne R S Adriaanse, Romy S Bos, Manuel Torres-Diz, Stephen P Hunger, Kathryn G Roberts, Charles G Mullighan, Ronald W Stam, Andrei Thomas-Tikhonenko, Justo P Castaño, Raúl M Luque, Eduardo Eyras
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摘要

由于尚未确定的机制,相当大比例的婴儿b细胞急性淋巴细胞白血病(B-ALL)患者仍然预后不佳。我们对基因表达、基因融合和RNA剪接改变进行了全面的多队列分析,以揭示可能与观察到的不良结果相关的分子特征。我们确定了87种融合,这些融合在患者中具有显著的等位基因频率,并具有共同的功能影响,表明融合的共同机制。我们进一步确定了一个独立于基因融合背景预测高风险的基因表达特征,包括剪接因子SRRM1的上调。在B-ALL细胞系中的实验进一步证明了SRRM1在细胞存活、增殖和侵袭中的作用。补充分析显示,SRRM1可能通过与其他剪接因子的蛋白质相互作用来调节与不良预后相关的剪接事件。我们的研究结果揭示了异常RNA加工的潜在趋同机制,该机制独立于潜在的基因融合维持恶性表型,并且可能潜在地补充当前婴儿B-ALL的临床策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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A convergent malignant phenotype in B-cell acute lymphoblastic leukemia involving the splicing factor SRRM1.

A significant proportion of infant B-cell acute lymphoblastic leukemia (B-ALL) patients remains with a dismal prognosis due to yet undetermined mechanisms. We performed a comprehensive multicohort analysis of gene expression, gene fusions, and RNA splicing alterations to uncover molecular signatures potentially linked to the observed poor outcome. We identified 87 fusions with significant allele frequency across patients and shared functional impacts, suggesting common mechanisms across fusions. We further identified a gene expression signature that predicts high risk independently of the gene fusion background and includes the upregulation of the splicing factor SRRM1. Experiments in B-ALL cell lines provided further evidence for the role of SRRM1 on cell survival, proliferation, and invasion. Supplementary analysis revealed that SRRM1 potentially modulates splicing events associated with poor outcomes through protein-protein interactions with other splicing factors. Our findings reveal a potential convergent mechanism of aberrant RNA processing that sustains a malignant phenotype independently of the underlying gene fusion and that could potentially complement current clinical strategies in infant B-ALL.

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