TY - EJOU AU - Fang, Li-Zhou AU - Zhang, Jian-Qing AU - Liu, Ling AU - Fu, Wei-Ping AU - Shu, Jing-Kui AU - Feng, Jia-Gang AU - Liang, Xiao TI - Silencing of Btbd7 Inhibited Epithelial–Mesenchymal Transition and Chemoresistance in CD133+ Lung Carcinoma A549 Cells T2 - Oncology Research PY - 2017 VL - 25 IS - 5 SN - 1555-3906 AB - 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. KW - Btbd7; CD133+; Epithelial–mesenchymal transition (EMT); Chemoresistance; Non-small cell lung cancer (NSCLC) DO - 10.3727/096504016X14772349843854