期刊
IN VITRO CELLULAR & DEVELOPMENTAL BIOLOGY-ANIMAL
卷 58, 期 1, 页码 37-43出版社
SPRINGER
DOI: 10.1007/s11626-021-00638-7
关键词
ESCC; NRON; miR-31; Cisplatin; Apoptosis
资金
- Medical Innovation Fund of Fujian Health Administration [2016-CX-31]
- Natural Science Foundation of Fujian Province, China [2020J01953]
- Young and Middle-aged Teachers Scientific Research Project of Education Department, Fujian Province, China [JAT190212]
This study found that NRON may promote the development of cisplatin resistance in esophageal squamous cell carcinoma (ESCC) by downregulating the expression of miR-31.
LncRNA non-coding repressor of NFAT (NRON) can promote bladder cancer and suppress liver cancer, while its role in esophageal squamous cell carcinoma (ESCC) is unknown. We analyzed its involvement in ESCC. NRON and miR-31 expression in plasma before and after cisplatin treatment was detected using RT-qPCR. The correlation between NRON and miR-31 was analyzed by linear regression. Expression of NRON and miR-31 in ESCC cells was also analyzed using RT-qPCR. Overexpression of NRON and miR-31 was achieved in ESCC cells to explore their interaction. Cell apoptosis induced by cisplatin was studied using cell apoptosis assay. NRON was highly expressed in ESCC and further upregulated after cisplatin treatment. MiR-31 was downregulated in ESCC and inversely correlated with NRON. In ESCC cells, NRON overexpression decreased miR-31 expression, while miR-31 failed to alter NRON expression. Cisplatin treatment promoted NRON expression and inhibited miR-31 expression. Under cisplatin treatment, cell apoptosis was inhibited after NRON overexpression and increased after miR-31 overexpression. Moreover, NRON inhibited the effect of miR-31 on cell apoptosis. NRON might promote the development of cisplatin resistance via downregulating miR-31 in ESCC.
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