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MiR-129-5p inhibits liver cancer growth by targeting calcium calmodulin-dependent protein kinase IV (CAMK4)

机译:MiR-129-5p通过靶向钙调蛋白依赖性蛋白激酶IV(CAMK4)抑制肝癌的生长

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摘要

This study was designed to investigate the mechanism by which miR-129-5p affects the biological function of liver cancer cells. The expression levels of miR-129–5p in liver cancer tissues and cells were, respectively, determined. Crystal violet staining and flow cytometry were used to detect cell proliferation and apoptosis. Wound healing assay and transwell assay were performed to test cell migration and invasion. The target gene of miR-129–5p was analyzed and verified by bioinformatics analysis and luciferase reporter assay. Tumorigenicity assays in nude mice were used to test the antitumor ability of calcium calmodulin-dependent protein kinase IV (CAMK4). miR-129–5p was found to be underexpressed in hepatocellular cancer tissues and cells and also to inhibit liver cells proliferation, migration, and invasion and promote apoptosis. CAMK4 was a direct target for miR-129–5p and was lowly expressed in liver cancer tissues and cells. CAMK4 was also found to inhibit liver cells proliferation, migration and invasion, and promote apoptosis. CAMK4 might exert an antitumor effect by inhibiting the activation of mitogen-activated protein kinase (MAPK). MiR-129–5p was a tumor suppressor with low expression in liver cancer tissues and cells. CAMK4, which is a direct target gene of miR-129–5p, could inhibit tumor by inhibiting the activation of MAPK signaling pathway.
机译:本研究旨在研究miR-129-5p影响肝癌细胞生物学功能的机制。确定了miR-129-5p在肝癌组织和细胞中的表达水平。结晶紫染色和流式细胞仪用于检测细胞增殖和凋亡。进行伤口愈合测定和transwell测定以测试细胞迁移和侵袭。 miR-129-5p的靶基因已通过生物信息学分析和荧光素酶报告基因分析进行了分析和验证。裸鼠的致瘤性试验用于测试钙调蛋白依赖性蛋白激酶IV(CAMK4)的抗肿瘤能力。发现miR-129-5p在肝细胞癌组织和细胞中表达不足,并且还抑制肝细胞的增殖,迁移和侵袭并促进凋亡。 CAMK4是miR-129-5p的直接靶标,在肝癌组织和细胞中低表达。还发现CAMK4抑制肝细胞增殖,迁移和侵袭,并促进细胞凋亡。 CAMK4可能通过抑制有丝分裂原激活的蛋白激酶(MAPK)的激活而发挥抗肿瘤作用。 MiR-129-5p是在肝癌组织和细胞中低表达的肿瘤抑制因子。 CAMK4是miR-129-5p的直接靶基因,可以通过抑制MAPK信号通路的激活来抑制肿瘤。

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