极性蛋白SCRIB的截断形式通过调节几种信号通路成分诱导MDA-MB231细胞凋亡

Joseph Papamathekis
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引用次数: 0

摘要

极性蛋白是建立和维持乳腺组织完整性的基础,而其氨基酸序列和蛋白质结构的改变可以驱动乳腺癌的形成和进展。Scrib是一种多功能支架蛋白,其在细胞内的正确定位对其正确发挥功能至关重要。我们在这里报道了LRR结构域极性蛋白的截断形式的异位表达,驱动MDA-MB231乳腺癌细胞发生caspase 3介导的凋亡细胞死亡。此外,我们发现截断的Scrib是JNK/c-Jun, Notch和Wnt/β-catenin信号通路的调节因子。我们的研究结果表明,在具有特定基因突变背景(KRAS, AFRGAP1, BRAF, MYCL)的乳腺癌细胞系中,截断的Scrib的异位表达激活了细胞内分子改变程序并促进了细胞凋亡。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Truncated Form of the Polarity Protein SCRIB Induces Apoptosis in MDA-MB231 Cells by Regulating Components of Several Signalling Pathways
Polarity proteins are fundamental to the establishment and maintenance of breast tissue integrity, whereas alterations of their amino acid sequence and protein structure can drive breast cancer formation and progression. Scrib is a multi-functional scaffold protein whose proper localization within the cell is pivotal for its correct function. We report here that the ectopic expression of a truncated form of the polarity protein of the LRR domain, drives MDA-MB231 breast cancer cells to caspase 3-mediated apoptotic cell death. Furthermore, we identify the truncated Scrib as a regulator of JNK/c-Jun, Notch and Wnt/β-catenin signalling pathways. Our results indicate that the ectopic expression of the truncated Scrib in a breast cancer cell line with a specific background of genetic mutations (KRAS, AFRGAP1, BRAF, MYCL) activates a program of intracellular molecular alterations and promotes apoptosis.
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