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Cancer Lett. 2012 Apr 28;317(2):184-91. doi: 10.1016/j.canlet.2011.11.024. Epub 2011 Nov 25.

MiR-100 resensitizes docetaxel-resistant human lung adenocarcinoma cells (SPC-A1) to docetaxel by targeting Plk1.

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1
Department of Medical Oncology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, PR China.

Abstract

MicroRNAs (miRNAs) expression correlates with biological characteristics of both normal cells and cancer cells, but their roles in cancer chemoresistance remain unclear. By microarray analysis, miR-100 was found significantly down-regulated in docetaxel-resistant SPC-A1/DTX cells compared with parental SPC-A1 cells. Ectopic miR-100 expression resensitized SPC-A1/DTX cells to docetaxel by suppression of cell proliferation and induction of cell arrest in G(2)/M phase and apoptosis. Knock-down of Plk1, which was a direct target of miR-100, yielded similar effects as that of ectopic miR-100 expression. The inverse correlation between miR-100 and Plk1 expression was also detected in nude mice SPC-A1/DTX tumor xenografts and clinical lung adenocarcinoma tissues and was proved to be related with the in vivo response to docetaxel. Thus, our results suggested that down-regulation of miR-100 could lead to Plk1 over-expression and eventually to docetaxel chemoresistance of human lung adenocarcinoma.

PMID:
22120675
DOI:
10.1016/j.canlet.2011.11.024
[Indexed for MEDLINE]

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