MicroRNA-4513 Promotes Gastric Cancer Cell Proliferation and Epithelial–Mesenchymal Transition Through Targeting KAT6B

下调和上调 小RNA 上皮-间质转换 转染 免疫印迹 细胞生长 细胞培养 化学 癌症研究 细胞 生物 分子生物学 生物化学 基因 遗传学
作者
Huimin Ding,Yuhua Shi,Xiaobing Liu,Aifeng Qiu
出处
期刊:Human gene therapy. Clinical development [Mary Ann Liebert, Inc.]
卷期号:30 (3): 142-148 被引量:25
标识
DOI:10.1089/humc.2019.094
摘要

The purpose of this study was to investigate the expression level of microRNA-4513 (miR-4513) in gastric cancer (GC), and to elucidate the mechanisms underlying its regulation of GC progression. Quantitative real-time PCR (qRT-PCR) was performed to measure the expression level of miR-4513 in GC cells. Transfection efficacy of synthetic miRNAs was examined by qRT-PCR. After synthetic miRNA transfection, cell counting kit-8 assay and transwell invasion assay were conducted to measure biological changes in these groups. The key molecular expression level involved in epithelial-mesenchymal transition (EMT) was analyzed by Western blot. Bioinformatic analysis and Western blot were performed to investigate the connection between miR-4513 and lysine acetyltransferase 6B (KAT6B). qRT-PCR results showed that miR-4513 expression level was upregulated in GC cell lines. Downregulation of miR-4513 expression inhibited GC cell proliferation, invasion, and EMT. KAT6B was validated as a direct target of miR-4513. In addition, KAT6B expression level can be upregulated by miR-4513 inhibitor. Collectively, we showed that miR-4513 is involved in regulating the biological function of GC cells via KAT6B. In addition, miR-4513 may serve as a potential target for the molecular therapy of GC.
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