1. Ambra1 inhibits paclitaxel-induced apoptosis in breast cancer cells by modulating the Bim/mitochondrial pathway
- Author
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Jie Luo, Zheng-wen Cai, Hua-wei Zhu, Wei-liang Sun, and Li Wang
- Subjects
Cancer Research ,Paclitaxel ,Chemistry ,Effector ,Autophagy ,Regulator ,Apoptosis ,Breast Neoplasms ,Mitochondrion ,medicine.disease ,Antineoplastic Agents, Phytogenic ,Mitochondria ,chemistry.chemical_compound ,Breast cancer ,Oncology ,Cell Line, Tumor ,Cancer cell ,medicine ,Cancer research ,Humans ,Adaptor Proteins, Signal Transducing - Abstract
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.
- Published
- 2019