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