索拉非尼通过抑制c-Myc和原胸腺素- α诱导肝癌细胞凋亡

Yi-Te Lin, C. Chao
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引用次数: 0

摘要

抗凋亡蛋白胸腺蛋白酶α (PTMA)在包括肝细胞癌(HCC)在内的多种癌症中过表达。早期的研究表明,PTMA通过抑制caspase-9的激活和凋亡体的形成来阻断癌细胞的凋亡。我们最近的研究表明,在索拉非尼治疗的HCC细胞中,PTMA的沉默增强了线粒体依赖的凋亡途径,导致Bax易位、pBad去磷酸化和细胞色素c释放。我们的研究结果还表明,pERK/c-Myc/Max/PTMA轴代表了索拉非尼在肝癌化疗中的一个新发现的靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sorafenib induces apoptosis in hepatocellular carcinoma cells by inhibiting c-Myc and prothymosin-alpha
The anti-apoptotic protein prothymosin alpha (PTMA) is overexpressed in various cancers, including hepatocellular carcinoma (HCC). Earlier studies have shown that PTMA blocks apoptosis in cancer cells by inhibiting caspase-9 activation and apoptosome formation. Our recent study shows that silencing of PTMA potentiates the mitochondria-dependent apoptosis pathway in sorafenib-treated HCC cells, leading to Bax translocation, pBad dephosphorylation, and cytochrome c release. Our findings also indicate that the pERK/c-Myc/Max/PTMA axis represents a newly identified target of sorafenib in chemotherapy against HCC.
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