Department of Gastroenterology, Yantai Municipal Laiyang Central Hospital, No. 111, Changshan Road, Laiyang City, Yantai 265200, Shandong Province, China.
J Biochem. 2021 Oct 12;170(3):337-347. doi: 10.1093/jb/mvab050.
LINC01207 is involved in the progression of some cancers. This study was designed to delve into the biological function and mechanism of LINC01207 in gastric cancer. Quantitative polymerase chain reaction (qPCR) was adopted to examine the expression levels of LINC01207, miR-671-5p, dead-box polypeptide 5 (DDX5) mRNA in gastric cancer tissues and cells. After LINC01207 was overexpressed or depleted, MTT and bromodeoxyuridine (BrdU) assays were conducted to detect cell proliferation. Transwell assay was employed to detect cell migration and invasion. Western blot was used to detect the expression of DDX5 protein in cells. Bioinformatics analysis, luciferase reporter assay and RNA pull-down assay were performed to predict and validate the binding site between miR-671-5p and LINC01207 or DDX5. LINC01207 and DDX5 mRNA were upregulated in gastric cancer, while miR-671-5p was downregulated; high expression of LINC01207 and transfection of miR-671-5p inhibitors facilitated the proliferation of gastric cancer cells; however, knocking down LINC01207 and the overexpression of miR-671-5p mimics had opposite biological effects. LINC01207 and miR-671-5p were interacted and miR-671-5p was negatively regulated by LINC01207. MiR-671-5p could reverse the function of LINC01207. DDX5 was a downstream target of miR-671-5p and was positively modulated by LINC01207. LINC01207 promotes the proliferation and metastasis of gastric cancer cells by regulating miR-671-5p/DDX5 axis.
LINC01207 参与了一些癌症的进展。本研究旨在深入研究 LINC01207 在胃癌中的生物学功能和机制。采用定量聚合酶链反应（qPCR）检测胃癌组织和细胞中 LINC01207、miR-671-5p、DEAD 框多肽 5（DDX5）mRNA 的表达水平。过表达或耗尽 LINC01207 后，通过 MTT 和溴脱氧尿苷（BrdU）检测细胞增殖。Transwell 检测用于检测细胞迁移和侵袭。Western blot 用于检测细胞中 DDX5 蛋白的表达。通过生物信息学分析、荧光素酶报告基因检测和 RNA 下拉实验预测和验证 miR-671-5p 与 LINC01207 或 DDX5 的结合位点。胃癌中 LINC01207 和 DDX5 mRNA 上调，而 miR-671-5p 下调；LINC01207 高表达和 miR-671-5p 抑制剂转染促进了胃癌细胞的增殖；然而，敲低 LINC01207 和过表达 miR-671-5p 模拟物则具有相反的生物学效应。LINC01207 和 miR-671-5p 相互作用，miR-671-5p 受 LINC01207 负调控。miR-671-5p 可以逆转 LINC01207 的功能。DDX5 是 miR-671-5p 的下游靶标，受 LINC01207 正向调控。LINC01207 通过调节 miR-671-5p/DDX5 轴促进胃癌细胞的增殖和转移。
