Overexpression of the erythropoietin receptor is associated with upregulation of tubulin beta 6 and paclitaxel resistance in ovarian adenocarcinoma cells.

The emergence of tumor 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 the T clone, which has a tendency to form spheroidal structures. In addition, functional enrichment analysis demonstrated that EPOR-associated differentially expressed genes are involved in several biological and cell processes. Indeed, a T clone with a single 68 kDa EPOR isotype demonstrates significant resistance to paclitaxel therapy and is associated with the upregulation of tubulin beta 6.