Decreased Expression of Enolase‐I Promotes Cisplatin Resistance of Ovarian Cancer Cells

Abstract

Platinum‐containing anticancer drugs has been used for more than four decades has effective treatment for ovarian cancer and many others solid tumors. However, the initial positive response to therapy is limited by development of resistance to cisplatin treatment. Although many mechanism of cisplatin resistance have been proposed, the molecular mechanism leading to the cisplatin resistance in ovarian cancer tumors has not fully understood. In this study, we sought to identify novel proteins associated with the cisplatin resistance of ovarian cancer cells. Quantitative proteomic analysis revealed low protein levels of Enolase‐1 (ENO1) in cisplatin resistant (A2780CP20) ovarian cancer cells compared to its counterpart cisplatin sensitive (A2780) cells. Small‐interference RNA (siRNA)‐targeted ENO1 showed a reduction in the sensitivity of ovarian cancer cells to cisplatin treatment. Contrasting, ectopic expression of ENO1 in cisplatin resistant ovarian cancer cells reduced the sensitivity of these cells to cisplatin treatment. Intracellular glucose uptake were measurements in pairs of cisplatin sensitive and cisplatin resistant cells. The glucose content levels were higher in all cisplatin resistant cells compared with their sensitive counterparts. Overall, these results suggest that low levels of ENO1 are associated with the cisplatin resistance of ovarian cancer cells. Therefore, targeting the glycolytic pathways could be a strategy to overcome the cisplatin resistance of women with advanced and drug resistant ovarian cancer.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.