Knockdown of Long Non-coding RNA HOTAIR Increases Cisplatin Sensitivity in Ovarian Cancer by Inhibiting Cisplatin-induced Autophagy

Purpose: Ovarian cancer is one of the most malignant tumors in the female reproductive system. With the widespread application of chemotherapeutic drugs, many ovarian cancer patients develop drug resistance. The aim of this study was to explore the function of HOTAIR in the treatment of ovarian cancer with cisplatin and its underlying mechanism.

Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect HOTAIR expressions in tissues and cells of ovarian cancer. Cell counting kit-8 (CCK-8) assay was used to examine the viability of ovarian cancer cells. Besides, small interfering (si) RNA was transfected to knockdown HOTAIR so as to explore its biological function. Western blot was performed to detect the expression levels of autophagy-related proteins. Flow cytometry was applied to detect apoptosis of ovarian cancer cells.

Results: HOTAIR was upregulated in ovarian cancer. Meanwhile, expression levels of autophagy-related proteins Atg7 and LC3 II/I in ovarian cancer cells increased with the increase of cisplatin concentration. Transfection of si-Atg7 could improve the therapeutic effect of cisplatin on ovarian cancer via inhibiting autophagy. Additionally, HOTAIR knockdown could increase the sensitivity of cisplatin in ovarian cancer treatment by inhibiting cisplatin-induced autophagy.

Conclusions: Knockdown of long non-coding (lnc) RNA HOTAIR could increase the sensitivity of cisplatin in ovarian cancer by inhibiting cisplatin-induced autophagy. Our research attempts to find a more effective treatment and provides new ideas for the clinical treatment of ovarian cancer.