TY -的A2 Roviello迈AU -林,林盟- Wang Yong PY - 2018 DA - 2018/12/23 TI - mir - 548 b - 3 - p调节增殖,凋亡和线粒体功能针对肝癌CIP2A SP - 7385426六世- 2018 AB - mir - 548 b的角色——3 - p在肝细胞癌(HCC)的发展仍未被发现的。本研究旨在探讨mir - 548 b的角色和机制在HCC - 3 - p。TCGA使用数据库,我们发现mir - 548 - p - b - 3表达低肝癌与正常组织相比,这进一步证实了RT-qPCR 20例手术切除的肝细胞癌和相应的正常组织。mir - 548 b - 3 - p模仿和抑制剂转染到Huh7 SK-Hep-1细胞,分别。MTT、集落形成和细胞周期分析显示,mir - 548 b - 3 - p模仿抑制细胞生长和细胞周期G1 / S过渡。相比之下,mir - 548 b - 3 - p抑制剂促进细胞生长和细胞周期的转变。mir - 548 b - 3 - p模仿也顺铂敏感性增加了移植细胞凋亡率。JC-1染色显示,mir - 548 b - 3 - p模仿表达下调的线粒体膜电位,而mir - 548 b - 3 - p在SK-Hep-1细胞抑制剂表现出相反的效果。使用预测软件,我们发现CIP2A的目标列表mir - 548 b - 3 - p。mir - 548 b - 3 - p模仿表达下调CIP2A及其下游靶蛋白原癌基因。 Luciferase reporter assay demonstrated that CIP2A was as a direct target of miR-548b-3p. CIP2A depletion partly reduced the effect of miR-548b-3p mimic/inhibitor on c-Myc. CIP2A depletion also reduced the effect of miR-548b-3p mimic/inhibitor on proliferation. In conclusion, our data demonstrated that miR-548b-3p was downregulated in HCC. miR-548b-3p regulates proliferation, apoptosis and mitochondrial function by targeting CIP2A in HCC. SN - 2314-6133 UR - https://doi.org/10.1155/2018/7385426 DO - 10.1155/2018/7385426 JF - BioMed Research International PB - Hindawi KW - ER -