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分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

circKMT2D contributes to H2O2‑attenuated osteosarcoma progression via the miR‑210/autophagy pathway

Jun Zhang, Xubin Chou, Ming Zhuang, Chenlei Zhu, Yong Hu, Dong Cheng, Zhiwei Liu

Journal:Experimental and Therapeutic Medicine

IF:1.79

DOI:10.3892/etm.2020.9193

PMID:32963595

Published:2020-09-09

research field:分子生物学细胞生物学癌症生物学

Abstract

Circular RNAs (circRNAs) have been demonstrated to be involved in osteosarcoma (OS) development; however, the underlying mechanism of circKMT2D in OS progression remains unclear. The present study aimed to elucidate how circKMT2D could affect hydrogen peroxide (H2O2)‑induced OS progression. H2O2 (100 µmol/l) was used to treat MG63 and U2OS cells. The cell viability, invasive ability, apoptosis and circKMT2D expression were detected using Cell Counting Kit‑8 assay, Transwell assay, flow cytometry and reverse transcription‑quantitative PCR, respectively. Furthermore, MG63 and U2OS cells transfected with circKMT2D short hairpin RNA and negative control were treated with H2O2, and circKMT2D expression and cell phenotype were determined. Dual‑luciferase reporter assay was conducted to determine the association between circKMT2D and miR‑210 expression level. Rescue experiments were conducted to examine the mechanisms through which circKMT2D and miR‑210 could affect H2O2‑treated MG63 cells. In addition, the effects of miR‑210 on the expression of the autophagy‑related proteins Beclin1 and p62 in H2O2‑treated MG63 cells were detected by western blotting. An autophagy inhibitor was used to treat the MG63 cells, and whether miR‑210 could affect the H2O2‑treated MG63 cell phenotype through autophagy was investigated. The results demonstrated that H2O2 treatment promoted cell apoptosis and decreased cell viability, invasive ability and circKMT2D expression in MG63 and U2OS cells. Furthermore, circKMT2D knockdown decreased the cell viability and invasive ability and enhanced the apoptosis of H2O2‑treated MG63 and U2OS cells. circKMT2D possessed binding sites for miR‑210 and inhibited miR‑210 expre

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