J Cancer 2016; 7(11):1557-1564. doi:10.7150/jca.15566
Bleomycin (BLM) Induces Epithelial-to-Mesenchymal Transition in Cultured A549 Cells via the TGF-β/Smad Signaling Pathway
1. Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing , 400042, PR China;
2. State Key Laboratory of Trauma, Burn and Combined Injury, Chongqing 400042 PR China;
3. Cancer Center, Daping Hospital and Research Institute of Surgery, Third Military Medical University, Chongqing, 400042, China.
* Kui-Jun Chen and Qing Li have contributed equally to this work.
Chen KJ, Li Q, Wen Cm, Duan ZX, Zhang Jy, Xu C, Wang JM. Bleomycin (BLM) Induces Epithelial-to-Mesenchymal Transition in Cultured A549 Cells via the TGF-β/Smad Signaling Pathway. J Cancer 2016; 7(11):1557-1564. doi:10.7150/jca.15566. Available from http://www.jcancer.org/v07p1557.htm
The epithelial-to-mesenchymal transition (EMT) is a crucial cellular event in wound healing, tissue repair, and cancer progression in adult tissues, with the interactions with numerous signals. In this study, we aimed to determine whether bleomycin (BLM), an agent that causes pulmonary fibrosis, induces the EMT of the alveolar epithelial cell line A549 and investigated the possible mechanisms. We examined the EMT involved changes in cell morphology, isoform switching of the fibroblast growth factor receptor 2 (FGFR2) by alternative splicing, and expression of the phenotypic markers including E-cadherin, vimentin, and α-SMA using RT-PCR, Western blotting, and immunofluorescence assays. A TGF-β/Smad inhibitor was used to determine whether coculture with BLM would inhibit the EMT of A549 cells. The results showed that BLM induced the EMT of A549 cells possibly via the TGF-β/Smad signaling pathway, evident from the decrease in the expression of E-cadherin and increase in the expression on vimentin.
Keywords: Bleomycin, Epithelial-to-Mesenchymal Transition, Pulmonary fibrosis, TGF-β.