期刊
ONCOLOGY REPORTS
卷 42, 期 3, 页码 1149-1160出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/or.2019.7222
关键词
erythropoietin receptor; paclitaxel resistance; breast cancer
类别
资金
- Scientific Grant Agency of the Ministry of Education of the Slovak Republic [VEGA1/0394/15, VEGA1/0536/19]
- Internal Scientific Grant System of the Faculty of Science of the Pavol Jozef Safarik University in Kosice [VVGS-PF-2016-72617]
- Operational Programme Research and Innovation - European Regional Development Fund [ITMS2014+ 313011D103]
While erythropoietin (EPO) regulates erythropoiesis, the erythropoietin receptor (EPOR) has been identified in many non-hematopoietic cells, including cancer. Our previous study demonstrated that overexpression of EPOR altered the cell growth and the sensitivity of RAMA 37 breast cancer cells to tamoxifen. Indeed, results of the present study uncovered the role of EPOR in the resistance of EPOR-overexpressing RAMA 37-28 cells to paclitaxel chemotherapy. In this regard, EPOR silencing in the presence of paclitaxel therapy decreased RAMA 37-28 cell proliferation, confirming its role in the sensitivity or resistance of RAMA 37-28 cells to paclitaxel. Notably, compared to parental RAMA 37 cells, RAMA 37-28 cells also showed a lower rate of apoptosis induced by paclitaxel, as monitored by caspase 3/7 activation and Annexin V by IncuCyte ZOOM system. Moreover, enhanced activation of signaling pathways mediated by pERK1/2 in RAMA 37-28 cells as detected by western blot analysis was demonstrated to be essential for paclitaxel resistance.
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