Chen Ziyuan, Chen Wei, Hong Zhiqi, Wu Xianqiao, Fang Tianzheng, Sheng Yufei, Fang Shuai, Zhou Chengwei
Department of Thoracic Surgery, The First Affiliated Hospital of Ningbo University, No. 59, Liuting Road, Haishu District, Ningbo, Zhejiang Province, China.
Health Science Center, Ningbo University, Ningbo, China.
J Cardiothorac Surg. 2024 Dec 23;19(1):679. doi: 10.1186/s13019-024-03160-5.
The regulatory role of the miR-618/JAK2/STAT3 axis in non-small cell lung cancer cells (NSCLC) was investigated with the objective of identifying a target for the precise treatment of patients with NSCLC.
Initially, differential gene expression was identified in the GEO database, followed by a comprehensive bioinformatics analysis. The tissue and cell levels of miR-618 were assessed using qRT-PCR, while the protein levels of JAK2 and STAT3 were determined through western blotting analysis. The association between miR-618 and JAK2 was scrutinized through bioinformatics analysis and dual-luciferase experiments. To evaluate cell proliferation, migration, and invasion, MTT, wound-healing, and Transwell assays were employed.
The expression of miR-618 is decreased in NSCLC, and it targets the JAK2/STAT3 pathway to inhibit the proliferation, invasion, and migration of NSCLC.
Our study demonstrates that a novel miR-618/JAK2/STAT3 signaling axis is involved in suppressing malignancy in NSCLC and provides a promising target for NSCLC therapy.
研究miR-618/JAK2/STAT3轴在非小细胞肺癌（NSCLC）细胞中的调控作用，旨在为NSCLC患者的精准治疗确定一个靶点。
首先在GEO数据库中鉴定差异基因表达，随后进行全面的生物信息学分析。使用qRT-PCR评估miR-618的组织和细胞水平，通过蛋白质免疫印迹分析确定JAK2和STAT3的蛋白质水平。通过生物信息学分析和双荧光素酶实验仔细研究miR-618与JAK2之间的关联。为评估细胞增殖、迁移和侵袭，采用MTT、伤口愈合和Transwell实验。
NSCLC中miR-618的表达降低，它靶向JAK2/STAT3通路以抑制NSCLC的增殖、侵袭和迁移。
我们的研究表明，一种新的miR-618/JAK2/STAT3信号轴参与抑制NSCLC的恶性肿瘤，并为NSCLC治疗提供了一个有前景的靶点。
