文献类型：期刊文献

英文题名：Postexercise downregulation of NUP155 in regulating non-small cell lung cancer progression via the PTEN/AKT signaling pathway

作者：Xu, Jiangang[1];Zhang, Liyin[1];Feng, Menghui[2];Hong, Weijun[3];Ye, Xinming[1]

机构：[1]East China Univ Sci & Technol, Sch Sports Sci & Engn, 130 Meilong Rd, Shanghai 200237, Peoples R China;[2]Shanghai Sport Univ, Wushu Coll, Dept Tradit Natl Sports, Shanghai, Peoples R China;[3]Minhang Cent Hosp, Dept Resp Med, Xinsong Rd, Shanghai 201100, Peoples R China

年份：2024

卷号：13

期号：11

起止页码：6323

外文期刊名：TRANSLATIONAL CANCER RESEARCH

收录：;WOS:【SCI-EXPANDED(收录号:WOS:001385974500006)】；

基金：Funding: This study was funded by the Research on Adolescent Mental and Brain Health Screening, Assessment, and Intervention (No. L110-72301) .

语种：英文

外文关键词：Exercise; non-small cell lung cancer (NSCLC); NUP155; PTEN/AKT signaling pathway; tumor progression

摘要：Background: Research interest into regulation of gene expression by physical activity and its effect on cancer prognosis has intensified. This study investigated the role of an exercise-related gene, NUP155, in the progression of non-small cell lung cancer (NSCLC) and its potential as therapy target. Methods: Using the GSE41914 dataset, which includes data related to exercise, and the Cancer Genome Atlas (TCGA)-NSCLC dataset, we identified differentially expressed genes (DEGs) and selected NUP155 as a hub gene for further analysis. NUP155 expression levels were measured in NSCLC cell lines and normal lung cells using in vitro assays. The functional roles of NUP155 were investigated through small interfering RNA (siRNA) knockdown experiments, assessing effects on migration, cell proliferation, invasion, and apoptosis. The involvement of the PTEN/AKT signaling pathway was examined using the PTEN inhibitor SF1670. Results: NUP155 was downregulated in postexercise samples and upregulated in NSCLC samples, indicating its association with poor prognosis in NSCLC. Knockdown of NUP155 in NSCLC cell lines resulted in reduced cell viability, migration, and invasion, alongside increased apoptosis. Western blotting revealed that NUP155 knockdown upregulated PTEN levels and downregulated phosphorylated AKT (p-AKT), without altering total AKT levels. The addition of SF1670 partially reversed the effects of NUP155 knockdown, indicating the involvement of the signaling pathway PTEN/AKT in NUP155-mediated tumorigenesis. Conclusions: NUP155 is upregulated in NSCLC, which promotes cell invasion and migration via the PTEN/AKT signaling pathway. Targeting NUP155, potentially influenced by exercise, could be a promising therapy. Combining exercise with targeted treatments may enhance patient outcomes.