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Published in: Tumor Biology 4/2016

01-04-2016 | Original Article

Rapamycin inhibited the function of lung CSCs via SOX2

Authors: Li-Xia Xie, Feng-Feng Sun, Bin-Feng He, Xiao-Feng Zhan, Juan Song, Sheng-Song Chen, Shi-Cang Yu, Xiao-Qun Ye

Published in: Tumor Biology | Issue 4/2016

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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
Title
Rapamycin inhibited the function of lung CSCs via SOX2
Authors
Li-Xia Xie
Feng-Feng Sun
Bin-Feng He
Xiao-Feng Zhan
Juan Song
Sheng-Song Chen
Shi-Cang Yu
Xiao-Qun Ye
Publication date
01-04-2016
Publisher
Springer Netherlands
Published in
Tumor Biology / Issue 4/2016
Print ISSN: 1010-4283
Electronic ISSN: 1423-0380
DOI
https://doi.org/10.1007/s13277-015-4341-y

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