Meng-Yao Sun1,2, Jian-Yong Zhu1, Chun-Yan Zhang1, Miao Zhang1, Ya-Nan Song1, Khalid Rahman3, Li-Jun Zhang4, Hong Zhang5,6. 1. Central Laboratory, Seventh People's Hospital of Shanghai, University of TCM, Shanghai, 200137, China. 2. Department of Pharmaceutical Botany, School of Pharmacy, Second Military Medical University, Shanghai, 200137, China. 3. Faculty of Science, School of Pharmacy and Biomolecular Sciences, Liverpool John Moores University, Liverpool, UK. 4. Central Laboratory, Seventh People's Hospital of Shanghai, University of TCM, Shanghai, 200137, China. zhanglijun0407@163.com. 5. Central Laboratory, Seventh People's Hospital of Shanghai, University of TCM, Shanghai, 200137, China. hqzhang51@126.com. 6. Department of Pharmaceutical Botany, School of Pharmacy, Second Military Medical University, Shanghai, 200137, China. hqzhang51@126.com.
Abstract
OBJECTIVES: To identify whether lncRNAs (long non-coding RNA) participate in the regulation of cisplatin-resistant induced autophagy in endometrial cancer cells. RESULTS: Autophagy activity was significantly boosted in cisplatin-resistant Ishikawa cells, a human endometrial cancer cell line, compared with that in parental Ishikawa cells. After analyzing the overall long noncoding RNA (lncRNA) profiling, a meaningful lncRNA, HOTAIR, was identified. It was down-regulated simultaneously in cisplatin-resistant Ishikawa cells and parental Ishikawa cells treated with cisplatin. RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR. CONCLUSIONS: It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of human endometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression.
OBJECTIVES: To identify whether lncRNAs (long non-coding RNA) participate in the regulation of cisplatin-resistant induced autophagy in endometrial cancer cells. RESULTS: Autophagy activity was significantly boosted in cisplatin-resistant Ishikawa cells, a humanendometrial cancer cell line, compared with that in parental Ishikawa cells. After analyzing the overall long noncoding RNA (lncRNA) profiling, a meaningful lncRNA, HOTAIR, was identified. It was down-regulated simultaneously in cisplatin-resistant Ishikawa cells and parental Ishikawa cells treated with cisplatin. RNA interference of HOTAIR reduced the proliferation of cisplatin-resistant Ishikawa cells and enhanced the autophagy activity of cisplatin-resistant Ishikawa cells with or without cisplatin treatment, in addition, beclin-1, multidrug resistance (MDR), and P-glycoprotein (P-gp) were mediated by lncRNA HOTAIR. CONCLUSIONS: It is clear that lncRNAs, specifically HOTAIR, can regulate the cisplatin-resistance ability of humanendometrial cancer cells through the regulation of autophagy by influencing Beclin-1, MDR, and P-gp expression.
Entities:
Keywords:
Autophagy; Cisplatin-resistance; Endometrial cancer; HOTAIR; Long noncoding RNA