Sam 68 overexpression desensitizes of ovarian cancer cells to cisplatin via promoting Cyclin D 1 b

Multiple oncoproteins have been identified to correlate with the chemoresistance in epithelial ovarian cancer (EOC). Src-associated in mitosis (Sam68) is a signaling marker in the transduction and activation of RNA family, and is also indicated to be oncogenic in multiple types of malignancies. However, it has not been recognized to contribute to the progression, recurrence and chemoresistance of EOC. This study was designed to investigate the expression of Sam68 in EOC OVCAR-3 and SK-OV-3 cells post the treatment with Cisplatin or Paclitacxel. And then we overexpressed Sam68 in SK-OV-3 cells to re-evaluate the cell sensitivity to Cisplatin via the colony forming assay, CCK-8 assay and apoptosis analysis. In addition, the expression of Cyclin D1a and D1b was examined in the abovementioned SK-OV-3 cells. Results demonstrated that Sam68 was downregulated by the treatment with Cisplatin or Paclitacxel in both cells. However, the Cisplatin-caused colony reduction and the growth reduction were markedly ameliorated by the Sam68 overexpression. Moreover, the Sam68 overexpression inhibits the cisplatin-promoted cellular viability reduction and apoptosis induction in SK-OV-3 cells. In addition, the downregulation of Cyclin D1b in the Cisplatin-treated EOC cells was also significantly blocked by the Sam68 overexpression. In conclusion, this study found the downregulation of Sam68 by Cisplatin treatment, and the Sam68 overexpression desensitizes ovarian cancer cells to cisplatin probably via promoting Cyclin D1b. It implies that Sam68 might be an effective target to optimize the chemosensitivity of EOC.