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Paclitaxel resistance is a critical challenge in ovarian cancer treatment. This study aimed to identify microRNAs (miRNAs) that modulate paclitaxel resistance for use as potential therapeutic targets in such settings. Paclitaxel-resistant cell lines were established using two ovarian cancer cell lines: SKOV3ip1 and HeyA8. The evaluation of miRNA polymerase chain reaction (PCR) arrays indicated that the expression of miR-522-3p was downregulated in paclitaxel-resistant cells. The restoration of miR-522-3p sensitized the resistant cells to paclitaxel, and its downregulation desensitized the parental cells. Using PCR arrays, we focused on  E2F2,  with the luciferase reporter assay revealing that it was a direct target for miR-522-3p. The paclitaxel-resistant cells showed stronger  E2F2  expression than the parental cells, while  E2F2  inhibition sensitized the resistant cells to paclitaxel. Forced  E2F2  expression in the parental cells led to the acquisition of paclitaxel resistance, while miR-522-3p inhibited  E2F2  expression and was associated with retinoblastoma protein phosphorylation attenuation, which resulted in G0/G1 arrest. The effects of miR-522-3p and  E2F2  in ovarian cancer were examined using public databases, revealing that low miR-522-3p expression and high  E2F2  expression were associated with significantly poorer overall survival. In conclusion, miR-522-3p attenuated the degree of paclitaxel resistance in vitro through the downregulation of  E2F2;  miR-522-3p supplementation may be a therapeutic target for paclitaxel-resistant ovarian cancer.

Paclitaxel exposure downregulates miR-522 expression and its downregulation induces paclitaxel resistance in ovarian cancer cells