相互作用体
细胞凋亡
细胞培养
流式细胞术
分子生物学
转染
庆大霉素保护试验
A549电池
生物
腺癌
癌症研究
细胞
免疫印迹
小RNA
化学
癌症
基因
遗传学
作者
Tao Peng,Fan Yang,Zhanwen Sun,Jie Yan
标识
DOI:10.1089/cbr.2020.4456
摘要
Background: TEK and miR-19a-3p have been reported to regulate lung adenocarcinoma (LUAD) progression. However, the association between TEK and miR-19a-3p in LUAD remained unknown. This research investigated a novel miR-19a-3p/TEK interactome in LUAD cells. Materials and Methods: The mRNA expression and protein expression in the cell lines were determined using qPCR and Western blot assay, respectively. CCK-8 assay, EDU assay, flow cytometry cell apoptosis assay, scratch assay, and cell-to-extracellular matrix adhesion assay were performed to detect the proliferation, apoptosis, migration, and adhesion ability of A549 and H1975 cell lines. Results: Findings revealed that both mRNA and protein levels of TEK were downregulated in the LUAD tumor tissues and cell lines. It was also found that compared with the control group, the transfection of TEK overexpression plasmids into H1975 and A549 cell lines significantly inhibited cancerous phenotypes. However, experimental results indicated that by downregulating TEK, miR-19a-3p promoted LUAD cell phenotypes. Conclusion: This research demonstrated that an interactome existed between miR-19a-3p and TEK and that miR-19a-3p could suppress LUAD tumors by inhibiting TEK. This novel interactome could be used as a novel therapy target for LUAD.
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