Open AccessSilencing of Btbd7 Inhibited Epithelial‐Mesenchymal Transition and Chemoresistance in CD133+ Lung Carcinoma A549 Cells
Author(s) -
Li-Zhou Fang,
Jianqing Zhang,
Ling Liu,
Wei Fu,
Jing-Kui Shu,
Jia-Gang Feng,
Liang Xiao
Publication year - 2017
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504016x14772349843854
Subject(s) - cancer stem cell , cancer research , epithelial–mesenchymal transition , a549 cell , carcinogenesis , gene silencing , lung cancer , stem cell , downregulation and upregulation , cancer , biology , cancer cell , chemistry , medicine , pathology , microbiology and biotechnology , metastasis , genetics , gene
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.