Silencing of BTBD7 inhibited epithelial-mesenchymal transition and 6 chemoresistance in CD133+ lung carcinoma A549 cells.

Abstract lpgCancer stem cell (CSC) are responsible for the tumorigenesis and recurrence, so targeting CSCs is a potentialeffective method to cure cancers. 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 were still unknown.l/pglpgTherefore, in this study, we first found that the radio of tumor sphere formation and stem cell transcription factors in CD133+ cells were dramatically enhanced than parental cells, which indicated successfully sorting the CD133+ cells from A549. Meanwhile, Btbd7 and the markers of epithelial-mesenchymal transition process were expressed higher in CD133+ cells than parental cells. Silencing of Btbd7 was significantly inhibited the self-refreshing and epithelial-mesenchymal transition 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 suggested that Btbd7 is a promising agent to inhibit survival and chemoresistance of cancer stem-like cells of NSCLC, which may as an important therapeutic target in NSCLC.l/p>.