Department of Medical Oncology, The 2nd Affilliated Hospital of Harbin Medical University, Harbin, China.
Eur Rev Med Pharmacol Sci. 2018 Feb;22(4):1011-1019. doi: 10.26355/eurrev_201802_14383.
To identify the functioning mode of miR-378 on non-small cell lung cancer (NSCLC) and provide therapeutic targets for NSCLC.
Expression levels of miR-378 in human NSCLC tissue samples and NSCLC-derived cell lines were measured by using quantitative Real-time polymerase chain reaction (PCR). Cell proliferation capacity was assessed by methyl thiazolyl tetrazolium (MTT) assay and colony formation assay. Cell apoptosis and cell cycle distribution were identified by flow cytometry. Downstream target gene was confirmed by using luciferase and Western blotting assays.
MiR-378 was significantly elevated in NSCLC tissues when compared with para-carcinoma tissues (n=42). Decreased-miR-378 could attenuate cell proliferation capacity, as well as promoted cell apoptosis and induced cell cycle arrest at G0/G1 phase. FOXG1 was chosen as the target gene of miR-378 by bioinformatics analysis and luciferase reporter assay. Moreover, restoration of miR-378 could impair the tumor suppression role of downregulated-miR-378 on NSCLC growth.
Decreased-miR-378 exerted tumor-suppressive effects on NSCLC growth via targeting FOXG1 in vitro, which provided an innovative and candidate target for diagnosis and treatment of NSCLC.
鉴定 miR-378 在非小细胞肺癌（NSCLC）中的作用模式，为 NSCLC 提供治疗靶点。
采用实时定量聚合酶链反应（PCR）检测人 NSCLC 组织样本和 NSCLC 衍生细胞系中 miR-378 的表达水平。通过甲基噻唑基四唑（MTT）测定和集落形成测定评估细胞增殖能力。通过流式细胞术鉴定细胞凋亡和细胞周期分布。通过荧光素酶和 Western blot 测定证实下游靶基因。
与癌旁组织相比（n=42），NSCLC 组织中 miR-378 显著升高。降低 miR-378 可减弱细胞增殖能力，促进细胞凋亡，并诱导细胞周期停滞在 G0/G1 期。通过生物信息学分析和荧光素酶报告基因测定，FOXG1 被选为 miR-378 的靶基因。此外，恢复 miR-378 可削弱下调 miR-378 对 NSCLC 生长的肿瘤抑制作用。
降低 miR-378 通过靶向 FOXG1 在体外对 NSCLC 生长发挥肿瘤抑制作用，为 NSCLC 的诊断和治疗提供了创新的候选靶点。
