Chen Xiaoyan, Su Shanna, Liu Jingyi, Zhang Dong, Qiang Guangliang
Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Baotou Medical College, No. 41 Linyin Road, Baotou, 014010, China.
Department of Thoracic Surgery, Peking University Third Hospital, Beijing, China.
Discov Oncol. 2025 Jun 4;16(1):1002. doi: 10.1007/s12672-025-02564-6.
This study aimed to investigate the expression and role of miR-17-5p in lung cancer.
The levels of miR-17-5p in four non-small cell lung cancer cell lines and human normal lung epithelial cells (BEAS-2B) were detected by fluorescent quantitative PCR. Next, the cell lines with relatively high expression of miR-17-5p were treated with miR-17-5p mimics, miR-17-5p inhibitor or control miRNA. CCK8, flow cytometry analysis, and Transwell assay were used to analyze cell proliferation, apoptosis, invasion, and migration. The target genes of miR-17-5p were predicted based on Starbase and Targetscan databases, and the interaction between miR-17-5p and SIK1 was verified by luciferase assay.
miR-17-5p was highly expressed in lung cancer tissues of patients with lung cancer. Overexpression of miR-17-5p significantly promoted lung adenocarcinoma cell proliferation, invasion, and migration, and inhibited apoptosis. There was a direct binding site between miR-17-5p and SIK1 3'UTR, and overexpression of miR-17-5p inhibited the expression of SIK1 at both mRNA and protein levels.
Our findings suggest that miR-17-5p may promote lung adenocarcinoma by targeting SIK1 and may be a potential biomarker for lung cancer.
本研究旨在探讨miR-17-5p在肺癌中的表达及作用。
采用荧光定量PCR检测四种非小细胞肺癌细胞系及人正常肺上皮细胞（BEAS-2B）中miR-17-5p的水平。接下来，对miR-17-5p表达相对较高的细胞系分别用miR-17-5p模拟物、miR-17-5p抑制剂或对照miRNA进行处理。采用CCK8、流式细胞术分析及Transwell实验分析细胞增殖、凋亡、侵袭及迁移情况。基于Starbase和Targetscan数据库预测miR-17-5p的靶基因，并通过荧光素酶实验验证miR-17-5p与SIK1之间的相互作用。
miR-17-5p在肺癌患者的肺癌组织中高表达。miR-17-5p的过表达显著促进肺腺癌细胞的增殖、侵袭及迁移，并抑制细胞凋亡。miR-17-5p与SIK1 3'UTR之间存在直接结合位点，miR-17-5p的过表达在mRNA和蛋白水平均抑制SIK1的表达。
我们的研究结果表明，miR-17-5p可能通过靶向SIK1促进肺腺癌发生，可能是肺癌的潜在生物标志物。
