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Rapamycin inhibited the function of lung CSCs via SOX2

Xie, Li-Xia, Sun, Feng-Feng, He, Bin-Feng, Zhan, Xiao-Feng, Song, Juan, Chen, Sheng-Song, Yu, Shi-Cang, Ye, Xiao-Qun·2016·Tumor Biology

Abstract

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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Metadata

Authors
Xie, L.-X., Sun, F.-F., He, B.-F., Zhan, X.-F., Song, J., Chen, S.-S., Yu, S.-C., & Ye, X.-Q.
Venue
Tumor Biology
Published
2015-11-03
Volume
37
Issue
4
Pages
4929-4937
ISSN
  • 1010-4283
  • 1423-0380
Cited by
12
References
1
Language
en
Funders
  • National Natural Science Foundation of China (CN) (81160277)
  • Major scientific and technological projects of Jiangxi Province (20143ACB20011)
  • General Project on Social Development by Department of Science and Technology of Jiang Xi Province (20141BBG70035)

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CoChat. (2026). Citation check: Rapamycin inhibited the function of lung CSCs via SOX2. https://app.cochat.ai/papers/10.1007/s13277-015-4341-y
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Xie, L.-X., Sun, F.-F., He, B.-F., Zhan, X.-F., Song, J., Chen, S.-S., Yu, S.-C., & Ye, X.-Q. (2016). Rapamycin inhibited the function of lung CSCs via SOX2. Tumor Biology. https://doi.org/10.1007/s13277-015-4341-y