目的 本研究拟揭示周期性应力刺激与肺癌发生发展的潜在机制。 方法 本研究通过重分析GEO数据库中的数据集GSE272292，初步探讨了硬基质环境下周期性拉伸应力（15%应变，0.2 Hz，持续7 d）对肺腺癌细胞A549基因表达调控的影响。 结果 功能富集分析显示，差异基因显著富集于能量代谢的重要场所“线粒体内膜”和“含胶原的细胞外基质”，并筛选出线粒体核糖体蛋白（MRPL13）和V型胶原蛋白（COL5A1）作为调控该双表型的关键候选基因。GSEA分析进一步揭示了“CD22介导的B细胞受体信号调控”通路激活。 结论 机械信号可能通过调控MRPL13和COL5A1分子介导肺癌细胞的线粒体能量代谢与细胞外基质重塑等表型改变，为肺癌机械生物学研究提供了新视角。
关键词：
机械拉伸; ; ; 肺癌; ; ; 线粒体代谢; ; ; 细胞外基质重塑
Objective To elucidate the potential mechanisms linking cyclic mechanical stress to lung tumorigenesis. Methods The GEO dataset GSE272292 was re-analyzed to investigate the effects of cyclic tensile stress (15% strain, 0.2 Hz, applied for 7 days) on gene expression in A549 lung adenocarcinoma cells under stiff matrix conditions. Results Functional enrichment analysis revealed that differentially expressed genes were significantly enriched in "mitochondrial inner membrane" (a hub for energy metabolism) and "collagen-containing extracellular matrix". Key candidate genes, including mitochondrial ribosomal protein (MRPL13) and collagen type V (COL5A1), were identified as regulators of these dual phenotypes. GSEA further highlighted activation of "CD22-mediated B-cell receptor signaling regulation" pathway. Conclusions These findings suggest that mechanical signals may drive phenotypic alterations in mitochondrial energy metabolism and extracellular matrix (ECM) remodeling via MRPL13 and COL5A1, offering novel insights into lung cancer mechanobiology.
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鈥�樊庭宇，讲师，E-mail: 526201753@qq.com；宫凤英，副主任医师，E-mail: gfying2011@smu.edu.cn
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