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首页> 外文期刊>Journal of Cellular Physiology >A NOXA/MCL-1 Imbalance Underlies Chemoresistance of Malignant Rhabdoid Tumor Cells
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A NOXA/MCL-1 Imbalance Underlies Chemoresistance of Malignant Rhabdoid Tumor Cells

机译：病因/ mcl1失衡基础化学抗性恶性肿瘤细胞杆状的

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摘要

Malignant rhabdoid tumor (MRT) is a rare aggressive pediatric cancer characterized by inactivation of SNF5, a core subunit of SWI/SNF complexes. Previously, we showed that SNF5 contributes to transcriptional activation of NOXA, a pro-apoptotic protein that binds and inhibits the anti-apoptotic protein MCL-1. In this study, we found that NOXA expression was downregulated in MRT cell lines as well as in clinical MRT samples and that ectopically expressed NOXA bound MCL-1 and increased the sensitivity of MRT cell lines to doxorubicin (DOX) by promoting apoptosis. Consistent with this finding, knockdown of MCL-1 in MRT cell lines induced apoptosis and increased DOX sensitivity in MRT cells, and the MCL-1 inhibitor TW-37 synergized with DOX to induce MRT cell death. Our results suggest that modulation of the NOXA/MCL-1 pathway may be a potential strategy for the treatment of patients with MRT. (C) 2015 Wiley Periodicals, Inc.
机译：(捷运)是一种罕见的恶性杆状的肿瘤积极的儿科癌症的特征SNF5失活,瑞士/ SNF的核心单元复合物。导致转录激活病因,pro-apoptotic蛋白结合抑制抗凋亡蛋白mcl1。这项研究中,我们发现病因表达式在捷运细胞系以及表达下调临床,ectopically捷运样品表达了病因mcl1和增加了阿霉素的敏感性捷运细胞系(阿霉素)通过促进细胞凋亡。这一发现,击倒mcl1的捷运细胞诱导细胞凋亡,增加阿霉素在捷运细胞敏感性,mcl1抑制剂TW-37主体性与阿霉素诱导细胞捷运死亡。病因/ mcl1通路可能是一个潜在的战略治疗患者的捷运。威利期刊公司。

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