Overexpression of erythropoietin receptor causes paclitaxel resistance in ovarian adenocarcinoma cells

The emergence of tumour cell resistance is one of the major issues in current oncology practice. It reduces the effectiveness of therapy and worsens cancer patients' prognoses. However, it confirms a wide range of molecular interactions as well as the complexity of the human organism. Our previous research confirmed the functionality of the erythropoietin receptor (EPOR) in ovarian and breast cancer cells, as well as its relationship to these cells' sensitivity to specific therapies. The current study demonstrates that EPOR overexpression in human ovarian adenocarcinoma cells A2780 is directly linked to paclitaxel resistance. Furthermore, EPOR overexpression results in morphological changes that vary according to the pattern of EPOR isotypes expressed. In this regard, the most interesting result appears to be the change in the shape of T clone, which has a tendency to form spheroidal structures. Indeed, T clone with single 68 kDa EPOR isotype demonstrates also significant resistance to paclitaxel therapy.