Department of Thoracic Surgery, Nanhai Hospital of Southern Medical University (People's Hospital of Nanhai District), Foshan 528244, P.R. China.
Department of Oncology, Nanhai Hospital of Southern Medical University (People's Hospital of Nanhai District), Foshan 528244, P.R. China.
Biosci Rep. 2019 Jan 18;39(1). doi: 10.1042/BSR20180855. Print 2019 Jan 31.
Non-small cell lung cancer (NSCLC) is one of the most fatal types of cancer with significant mortality and morbidity worldwide. MicroRNAs (miRs) have been confirmed to have positive functions in NSCLC. In the present study, we try to explore the role of miR-758 in proliferation, migration, invasion, and apoptosis of NSCLC cells by regulating high-mobility group box (HMGB) 3 (HMGB3.) NSCLC and adjacent tissues were collected. Reverse transcription quantitative PCR (RT-qPCR) was employed to detect expression of miR-758 and HMGB3 in NSCLC and adjacent tissues, in BEAS-2B cells and NSCLC cell lines. The targetted relationship between miR-758 and HMGB3 was identified by dual luciferase reporter gene assay. The effects of miR-758 on proliferation, migration, invasion, cell cycle, and apoptosis of A549 cells. MiR-758 expression was lower in NSCLC tissues, which was opposite to HMGB3 expression. The results also demonstrated that miR-758 can target HMGB3. The cells transfected with miR-758 mimic had decreased HMGB3 expression, proliferation, migration, and invasion, with more arrested cells in G phase and increased apoptosis. Our results supported that the overexpression of miR-758 inhibits proliferation, migration, and invasion, and promotes apoptosis of NSCLC cells by negative regulating HMGB2. The present study may provide a novel target for NSCLC treatment.
非小细胞肺癌(NSCLC)是一种最致命的癌症类型,具有显著的全球死亡率和发病率。微小 RNA(miRs)已被证实对 NSCLC 具有积极作用。在本研究中,我们试图通过调节高迁移率族蛋白 B3(HMGB3)来探索 miR-758 在 NSCLC 细胞增殖、迁移、侵袭和凋亡中的作用。收集 NSCLC 及相邻组织,采用逆转录定量 PCR(RT-qPCR)检测 miR-758 和 HMGB3 在 NSCLC 及相邻组织、BEAS-2B 细胞和 NSCLC 细胞系中的表达。双荧光素酶报告基因检测鉴定 miR-758 与 HMGB3 的靶向关系。检测 miR-758 对 A549 细胞增殖、迁移、侵袭、细胞周期和凋亡的影响。miR-758 在 NSCLC 组织中表达降低,与 HMGB3 表达相反。结果还表明,miR-758 可以靶向 HMGB3。转染 miR-758 模拟物的细胞 HMGB3 表达降低,增殖、迁移和侵袭减少,G 期细胞阻滞增加,凋亡增加。我们的研究结果支持 miR-758 通过负调控 HMGB2 抑制 NSCLC 细胞的增殖、迁移和侵袭,并促进其凋亡。本研究可为 NSCLC 的治疗提供新的靶点。