Wu Kai, Yang Liucheng, Chen Jianfeng, Zhao Haijun, Wang Jianjun, Xu Shuai, Huang Zonghai
Department of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, China.
Department of General Surgery, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510282, China.
FEBS Lett. 2015 Jul 8;589(15):1911-9. doi: 10.1016/j.febslet.2015.05.056. Epub 2015 Jun 11.
miR-362-5p is down-regulated in high-risk neuroblastoma and can function as a tumor suppressor. However, its role remains poorly understood. We show that miR-362-5p is down-regulated in metastatic neuroblastoma compared with primary neuroblastoma. Overexpression of miR-362-5p inhibits cell proliferation, migration and invasion of neuroblastoma cells in vitro and suppresses tumor growth of neuroblastoma in vivo. Phosphatidylinositol 3-kinase (PI3K)-C2β is a target of miR-362-5p. Knockdown of PI3K-C2β by siRNA had a similar effect to overexpression of miR-362-5p on SH-SY5Y cells. Overexpression of PI3K-C2β partially reversed tumor-suppressive effects of miR-362-5p. We suggest that miR-362-5p suppresses neuroblastoma cell growth and motility, partially by targeting PI3K-C2β.
微小RNA-362-5p在高危神经母细胞瘤中表达下调，可作为肿瘤抑制因子发挥作用。然而，其作用仍知之甚少。我们发现，与原发性神经母细胞瘤相比，转移性神经母细胞瘤中微小RNA-362-5p表达下调。体外实验中，过表达微小RNA-362-5p可抑制神经母细胞瘤细胞的增殖、迁移和侵袭，体内实验中可抑制神经母细胞瘤的肿瘤生长。磷脂酰肌醇3-激酶（PI3K）-C2β是微小RNA-362-5p的一个靶点。用小干扰RNA敲低PI3K-C2β对SH-SY5Y细胞的作用与过表达微小RNA-362-5p相似。过表达PI3K-C2β可部分逆转微小RNA-362-5p的肿瘤抑制作用。我们认为，微小RNA-362-5p通过靶向PI3K-C2β部分抑制神经母细胞瘤细胞的生长和运动能力。
