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Rapamycin inhibited the function of lung CSCs via SOX2.

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机构: [1]Department of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China [2]Translational Research Center, North Sichuan Medical College, Nanchong, Sichuan 637000, People’s Republic of China [3]Institute of Pathology and Southwest Cancer Center, Southwest Hospital, Third Military Medical University, Chongqing 400037, China
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关键词: Lung cancer Cancer stem cell Rapamycin mTOR SOX2

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The presence of cancer stem cells (CSCs) is the source of occurrence, aggravation, and recurrence of lung cancer. Accordingly, targeting killing the lung CSCs has been suggested to be an effective approach for lung cancer treatment. In this study, we showed that rapamycin inhibited the mammalian target of rapamycin (mTOR) signal transduction in A549 cells and improved the sensitivity to cisplatin (DDP). The mechanisms involve inhibition of the SOX2 expression, cell proliferation, epithelial-mesenchymal transition (EMT) phenotype, and sphere formation. Interestingly, knocked down SOX2 was a similar effect with rapamycin in A549 sphere. Furthermore, we showed that ectopic expression of Sox2 in A549 cells was sufficient to render them more resistant to rapamycin treatment in vitro. These data suggested that rapamycin inhibited the function of lung CSCs via SOX2. It will be of great interest to further explore the therapeutic strategies of lung cancer.

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出版当年[2016]版:
大类 | 3 区 医学
小类 | 3 区 肿瘤学
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第一作者机构: [1]Department of Respiratory Diseases, The Second Affiliated Hospital of Nanchang University, Nanchang 330006, China
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