Open Access

ARTICLE

Silencing of Btbd7 Inhibited Epithelial–Mesenchymal Transition and Chemoresistance in CD133⁺ Lung Carcinoma A549 Cells

Li-Zhou Fang^*, Jian-Qing Zhang^*, Ling Liu^*, Wei-Ping Fu^*, Jing-Kui Shu^*, Jia-Gang Feng^*, Xiao Liang^†

* Department of Respiratory Medicine, The First Affiliated Hospital of Kunming University of Science and Technology, Kunming City, Yunnan Province, P.R. China
† Department of Infectious Diseases, The First People’s Hospital of Yunnan Province, Kunming City, Yunnan Province, P.R. China

Oncology Research 2017, 25(5), 819-829. https://doi.org/10.3727/096504016X14772349843854

Abstract

Cancer stem cells (CSCs) are responsible for tumorigenesis and recurrence, so targeting CSCs is an effective method to potentially cure cancer. BTB/POZ domain-containing protein 7 (Btbd7) has been found in various cancers, including lung cancer and liver cancer, but the role of Btbd7 in non-small cell lung cancer (NSCLC), CSC self-renewal, and chemoresistance is still unknown. Therefore, in this study we found that the ratio of tumor sphere formation and stem cell transcription factors in CD133⁺ cells was dramatically enhanced compared to parental cells, which indicated successful sorting of CD133⁺ cells from A549. Meanwhile, Btbd7 and the markers of the epithelial–mesenchymal transition (EMT) process were more highly expressed in CD133⁺ cells than in parental cells. Silencing of Btbd7 significantly inhibited the self-renewal and EMT process in CD133⁺ cells. Furthermore, we found that downregulation of Btbd7 promoted cell apoptosis and increased the sensitivity to paclitaxel in CD133⁺ and parental cells. In conclusion, our results suggest that Btbd7 is a promising agent for the inhibition of survival and chemoresistance of cancer stem-like cells of NSCLC, which may act as an important therapeutic target in NSCLC.

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