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

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 ce...

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Detalles Bibliográficos
Autores principales: Fang, Li-Zhou, Zhang, Jian-Qing, Liu, Ling, Fu, Wei-Ping, Shu, Jing-Kui, Feng, Jia-Gang, Liang, Xiao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cognizant Communication Corporation 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7841122/
https://www.ncbi.nlm.nih.gov/pubmed/27983936
http://dx.doi.org/10.3727/096504016X14772349843854
Descripción
Sumario: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.