miR-15b 通过靶向 BCL2 增强肺腺癌的增殖和迁移。

miR-15b enhances the proliferation and migration of lung adenocarcinoma by targeting BCL2.

机构信息

Department of Thoracic Surgery, Yantai Affiliated Hospital of Binzhou Medical University, Yantai, China.

Department of Respiratory Medicine, Liaocheng Dongchangfu People's Hospital, Liaocheng, China.

出版信息

Thorac Cancer. 2020 Jun;11(6):1396-1405. doi: 10.1111/1759-7714.13382. Epub 2020 Mar 27.

BACKGROUND

Lung adenocarcinoma (LUAD) is a subtype of lung cancer (LC), which is the most common tumor worldwide. Accumulating evidence has elucidated an important role of microRNAs (miRNAs) in mediating the development and progression of several tumors. The purpose of this study was to explore the role and underlying mechanism of miR-15b in LUAD.

METHODS

CCK-8 and Transwell assays were conducted to measure the capacities of cell viability and migration in SPC-A1 cells. Luciferase assay was utilized to verifymiR-15b direct binding to BCL2 mRNA 3'-UTR.

RESULTS

We determined that miR-15b was overexpressed in LUAD and miR-15b overexpression predicted a significantly worse outcome in patients with LUAD. miR-15b improved LUAD growth in vitro and vivo. miR-15b enhanced cell migration and epithelial-mesenchymal transition (EMT) in LUAD. miR-15b promoted cell viability, migration and EMT through inhibiting BCL2 expression by targeting to its mRNA 3'-UTR. BCL2 reversed functions of miR-15b on promoting cell proliferation, migration and EMT in SPC-A1 cells.

CONCLUSIONS

miR-15b promoted cell viability, migration and EMT by targeting BCL2 in LUAD. The newly identified miR-15b/BCL2 axis provides a novel insight into the pathogenesis of LUAD.

背景

肺腺癌 (LUAD) 是肺癌 (LC) 的一种亚型，是全球最常见的肿瘤。越来越多的证据表明 microRNAs (miRNAs) 在介导几种肿瘤的发生和发展中起着重要作用。本研究旨在探讨 miR-15b 在 LUAD 中的作用及其潜在机制。

方法

使用 CCK-8 和 Transwell 测定法来测量 SPC-A1 细胞的细胞活力和迁移能力。利用荧光素酶测定来验证 miR-15b 是否直接结合 BCL2 mRNA 3'-UTR。

结果

我们确定 miR-15b 在 LUAD 中过表达，并且 miR-15b 过表达预测 LUAD 患者的预后明显较差。miR-15b 增强了 LUAD 在体外和体内的生长。miR-15b 增强了 LUAD 中的细胞迁移和上皮-间充质转化 (EMT)。miR-15b 通过靶向其 mRNA 3'-UTR 抑制 BCL2 表达，从而促进细胞活力、迁移和 EMT。BCL2 逆转了 miR-15b 在 SPC-A1 细胞中促进细胞增殖、迁移和 EMT 的功能。