Sustainability of CD24 expression, cell proliferation and migration, cisplatin-resistance, and caspase-3 expression during mesenchymal-epithelial transition induced by the removal of TGF-beta 1 in A549 lung cancer cells
Özet
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.
Sürdürülebilir Kalkınma Amaçları
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SKA 3: Sağlıklı Bireyler
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SKA 12: Sorumlu Üretim ve Tüketim
Atıf için künye
Kim, S., Park, J., Zhang, D., Cho, S., Yi, H., Cho, S., Chang, B., Kim, J., Shim, J., Hassıbelnaby, A. M. A., & Shin, H. (2017). Sustainability of CD24 expression, cell proliferation and migration, cisplatin-resistance, and caspase-3 expression during mesenchymal-epithelial transition induced by the removal of TGF-beta 1 in A549 lung cancer cells. ONCOLOGY LETTERS, 14(2), 2410–2416. https://doi.org/10.3892/ol.2017.6398
BibTeX
@article{kim2017-209935,
author = {Kim, Seong-Kwan and Park, Jin-A and Zhang, Dan and Cho, Sang-Hyun and Yi, Hee and Cho, Soo-Min and Chang, Byung-Joon and Kim, Jin-Suk and Shim, Jae-Han and Hassıbelnaby, Abdelaty Mostafa Abdelaty and Shin, Ho-Chul},
title = {Sustainability of CD24 expression, cell proliferation and migration, cisplatin-resistance, and caspase-3 expression during mesenchymal-epithelial transition induced by the removal of TGF-beta 1 in A549 lung cancer cells},
journal = {ONCOLOGY LETTERS},
year = {2017},
volume = {14},
number = {2},
pages = {2410--2416},
issn = {1792-1074},
doi = {10.3892/ol.2017.6398},
url = {https://akademik.atauni.edu.tr/yayinlar/209935-sustainability-of-cd24-expression-cell-proliferation-and-migration-cisplatin}
}