Department of Medical Oncology, The Second Affiliated Hospital, Guangxi Medical University, Nanning, China.
Neoplasma. 2019 May 23;66(3):377-385. doi: 10.4149/neo_2018_180710N467. Epub 2019 Feb 14.
Cancer cells often evade apoptosis induced by anti-cancer drugs, which reduces the efficacy of the drugs. Autophagy/Beclin 1 regulator 1 (Ambra1) is a crucial proautophagic protein. It also plays an important role in the execution of apoptosis. However, the mechanism by which Ambra1 regulates apoptosis has not been fully clarified. Moreover, whether Ambra1 participates in the regulation of paclitaxel-induced apoptosis in breast cancer cells is not clear. Here, we show that Ambra1 inhibits paclitaxel-induced apoptosis in breast cancer cells. Moreover, Bim and mitochondria are key effectors of Ambra1 in this process. Thus, Ambra1 is a protein that makes breast cancer cells resistant to apoptosis by modulating the Bim/mitochondrial pathway. Therefore, Ambra1 may be a potential target for the treatment of breast cancer.
癌细胞常常逃避抗癌药物诱导的细胞凋亡，从而降低药物的疗效。自噬/Beclin 1 调控蛋白 1（Ambra1）是一种关键的促自噬蛋白。它在细胞凋亡的执行中也起着重要作用。然而，Ambra1 调节细胞凋亡的机制尚未完全阐明。此外，Ambra1 是否参与调节乳腺癌细胞中紫杉醇诱导的细胞凋亡尚不清楚。在这里，我们表明 Ambra1 抑制乳腺癌细胞中紫杉醇诱导的细胞凋亡。此外，Bim 和线粒体是该过程中 Ambra1 的关键效应因子。因此，Ambra1 通过调节 Bim/线粒体途径使乳腺癌细胞对细胞凋亡产生抗性。因此，Ambra1 可能是治疗乳腺癌的潜在靶点。
