Open AccessEpithelialMesenchymal Transition Contributes to Docetaxel Resistance in Human Non-Small Cell Lung Cancer
Author(s) -
Weiwei Sui,
Hailin Pang,
Jiayu Liu,
Jianfeng Zhou,
Feng Zhang,
Lele Liu,
Ning Ma,
Ning Zhang,
Helong Zhang,
Huan Liu
Publication year - 2014
Publication title -
oncology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 57
eISSN - 1555-3906
pISSN - 0965-0407
DOI - 10.3727/096504014x14098532393473
Subject(s) - docetaxel , lung cancer , oncology , medicine , a549 cell , cancer research , vimentin , chemotherapy , immunohistochemistry
Lung cancer is an aggressive malignancy with high morbidity and mortality. Chemotherapy has always been the principal treatment measure, but its acquired resistance becomes a critical problem. In the current study, we established a new docetaxel-resistant human non-small lung cancer (NSCLC) cell line A549/Docetaxel. The resistance index (RI) of A549/Docetaxel cells and A549 induced by TGF- to docetaxel were 8.91 and 11.5, respectively. Compared to the parental A549 cells, the multiplication time of A549/Docetaxel was prolonged, the proportion of the cell cycle in the S phase decreased while that in the G 1 phase increased, and apoptotic rate was much lower. The morphology of the resistant cells eventuated epithelialmesenchymal transition (EMT), which was confirmed by the higher expression of fibronectin, vimentin (mesenchymal markers), and lower expression of E-cadherin (epithelial marker) at mRNA and proteins levels. Furthermore, the representative markers for docetaxel resistance were examined, including ABCB1 (MDR1), Bcl-2, Bax, and tubulin, to figure out the mechanisms of the resistance of A549/Docetaxel. In summary, we have established a typical docetaxel-resistant human NSCLC cell line A549/Docetaxel, and it was suggested that the multidrug resistance of A549/Docetaxel was related to EMT.