期刊
ONCOLOGY LETTERS
卷 14, 期 2, 页码 2410-2416出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2017.6398
关键词
transforming growth factor beta 1; epithelial-mesenchymal transition; mesenchymal-epithelial transition; caspase-3; cluster of differentiation 24; A549 lung cancer cell line
类别
资金
- Konkuk University [2015-A019-0076]
Epithelial-mesenchymal transition (EMT) is a notable mechanism underlying cancer cell metastasis. Transforming growth factor beta 1 (TGF-beta 1) has been used to induce EMT; however, there is a lack of information regarding the role of TGF-beta 1 in mesenchymal-epithelial transition (MET). In the present study, EMT was induced in A549 lung cancer cells using TGF-beta 1 (TGF-beta 1-treated group) and MET was induced sequentially from the TGF-beta 1-treated group by removing the TGF-beta 1 (MET/return group). Untreated A549 lung cancer cells were used as a control. Characteristic features, including cancer stem cell markers [cluster of differentiation (CD) 24, CD44 and CD133], cell proliferation and migration and diverse intracellular mechanisms, were observed in all groups. Using western blot analysis, the TGF-beta 1-treated group demonstrated increased vimentin and reduced E-cadherin expression, whereas the MET/return group demonstrated the opposite trend. Among cancer stem cell markers, the population of CD24(low) cells was reduced in the TGF-beta 1-treated group. Furthermore, the G2/M phase cell cycle population, cisplatin-sensitivity, and cell proliferation and migration ability were increased in the TGF-beta 1-treated group. These features were unaltered in the MET/return group when compared to the TGF-beta 1-treated group. Immunoblotting revealed an increase in the levels of SMAD3, phosphorylated SMAD3, phosphorylated extracellular signal-regulated kinase and caspase-3, and a decrease in active caspase-3 levels in the TGF-beta 1-treated group. Increased caspase-3 and reduced active caspase-3 levels were observed in the MET/return group, similar to those in the TGF-beta 1-treated group; however, levels of other signalling proteins were unchanged compared with the control group. EMT induced by TGF-beta 1 was not preserved; however, stemness-associated properties (CD24 expression, caspase-3 expression, cell proliferation and cisplatin-resistance) were sustained following removal of TGF-beta 1.
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