Cancer stem-like cells have cisplatin resistance and miR-93 regulate p21 expression in breast cancer
Autor: | Kanji Furuya, Akiko Sasaki, Yuko Tsunoda, Yuko Udaka, Mayumi Tsuji, Hideto Oyamada, Yuji Kiuchi, Nana Ichimura, Haruna Shirako, Masahiro Hosonuma |
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Rok vydání: | 2018 |
Předmět: |
Cisplatin
microRNA p21 biology CD24 CD44 Cancer General Medicine Cancer stem-like cells Cell cycle lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens medicine.disease lcsh:RC254-282 Cancer cell triple-negative breast cancer biology.protein Cancer research medicine Triple-negative breast cancer medicine.drug |
Zdroj: | Cancer Translational Medicine, Vol 4, Iss 2, Pp 48-53 (2018) |
ISSN: | 2395-3977 |
DOI: | 10.4103/ctm.ctm_41_17 |
Popis: | Aim: This study aims to examine the role of microRNAs (miRNAs) in regulating the expression of p21, a cyclin-dependent kinase inhibitor, and in inducing resistance to cisplatin, an anticancer drug. Methods: Human breast cancer cell line MDA-MB231 cells were separated into two subpopulations, cancer stem-like cells (CSCs) and cancer cells, based on the expression of cell surface antigens CD44 and CD24. Results: p21 protein expression was higher in CSCs than in cancer cells. Exposure of MDA-MB-231 cells to cisplatin increased p21 protein expression. However, p21 expression was significantly lower in cisplatin-treated CSCs than in cisplatin-treated cancer cells, suggesting that p21-dependent cell cycle suppression was lower in CSCs than in cancer cells. Moreover, caspase-3 activity was significantly lower in cisplatin-treated CSCs than in cisplatin-treated cancer cells, indicating that CSCs were more resistant to cisplatin-induced apoptosis than cancer cells. Treatment with miR-93 inhibitors increased p21 expression in CSCs, suggesting that miR-93 suppressed p21 expression. Conclusion: The results of the present study indicate that CSCs contribute to cisplatin resistance of MDA-MB231 cells and suggest that miR-93 inhibits the expression of p21, a factor involved in drug resistance. |
Databáze: | OpenAIRE |
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