MiR-23a-3p has been shown to promote liver cancer cell growth and metastasis and regulate that of chemosensitivity. Protocadherin17 (PCDH17) is a tumor suppressor gene and plays an essential part in cell cycle of hepatocellular carcinoma (HCC). This study aimed at evaluating the effects of miR-23a-3p and PCDH17 on HCC cell cycle and underlining the mechanism. The level of miR-23a-3p was up-regulated, while PCDH17 level was down-regulated in HCC tissues compared to adjacent tissues. For the in vitro studies, high expression of miR-23a-3p down-regulated PCDH17 level; increased cell viability; promoted G1/S cell cycle transition; up-regulated cyclin D1, cyclin E, CDK2, CDK4, p-p27, and p-RB levels; and down-regulated the expression of p27. Dual luciferase reporter assay suggested PCDH17 was a target gene of miR-23a-3p. MiR-23a-3p inhibitor and PCDH17 siRNA led to an increase in cell viability and the number of cells in the S phase and up-regulated cyclin D1 and cyclin E levels, compared with miR-23a-3p inhibitor and NC siRNA group. For the in vivo experiments, high expression of miR-23a-3p promoted tumor growth and reduced PCDH17 level in the cytoplasm. These results indicated that high expression of miR-23a-3p might promote G1/S cell cycle transition by targeting PCDH17 in HCC cells. The miR-23a-3p could be considered as a molecular target for HCC detection.

中文翻译：

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MiR-23a-3p通过靶向肝细胞癌中的procadadherin17促进G1 / S细胞周期转变。

MiR-23a-3p已显示出可促进肝癌细胞的生长和转移并调节化学敏感性。原钙粘蛋白17（PCDH17）是一种抑癌基因，在肝细胞癌（HCC）的细胞周期中起着至关重要的作用。这项研究旨在评估miR-23a-3p和PCDH17对HCC细胞周期的影响并强调其机制。与邻近组织相比，HCC组织中miR-23a-3p的水平上调，而PCDH17的水平下调。对于体外研究，miR-23a-3p的高表达下调了PCDH17的水平。细胞活力增加；促进G1 / S细胞周期转变；上调细胞周期蛋白D1，细胞周期蛋白E，CDK2，CDK4，p-p27和p-RB的水平; 并下调p27的表达。双重荧光素酶报告基因检测提示PCDH17是miR-23a-3p的靶基因。与miR-23a-3p抑制剂和NC siRNA组相比，MiR-23a-3p抑制剂和PCDH17 siRNA导致细胞活力和S期细胞数量增加，细胞周期蛋白D1和细胞周期蛋白E水平上调。对于体内实验，miR-23a-3p的高表达促进了肿瘤的生长并降低了细胞质中PCDH17的水平。这些结果表明，miR-23a-3p的高表达可能通过靶向HCC细胞中的PCDH17来促进G1 / S细胞周期转变。miR-23a-3p可被视为HCC检测的分子靶标。这些结果表明，miR-23a-3p的高表达可能通过靶向HCC细胞中的PCDH17来促进G1 / S细胞周期的转变。miR-23a-3p可被视为HCC检测的分子靶标。这些结果表明，miR-23a-3p的高表达可能通过靶向HCC细胞中的PCDH17来促进G1 / S细胞周期转变。miR-23a-3p可被视为HCC检测的分子靶标。