DataSheet3_Comprehensive analysis for clarifying transcriptomics landscapes of spread through air spaces in lung adenocarcinoma.xls

Patients with spread through air spaces (STAS) have worse postoperative survival and a higher recurrence rate in lung adenocarcinoma, even in the earliest phases of the disease. At present, the molecular pathogenesis of STAS is not well understood. Therefore, to illustrate the underlying pathogenic mechanism of STAS, we accomplished a comprehensive analysis of a microarray dataset of STAS. Differential expression analysis revealed 841 differentially expressed genes (DEGs) between STAS_positive and STAS_negative groups. Additionally, we acquired two hub genes associated with survival. Gene set variation analysis (GSVA) confirmed that the main differential signaling pathways between the two groups were hypoxia VHL targets, PKC, and pyrimidine metabolism pathways. Analysis of immune activity showed that the increased expression of MHC-class-Ⅰ was observed in the STAS_positive group. These findings provided novel insights for a better knowledge of pathogenic mechanisms and potential therapeutic markers for STAS treatment.

伴空气空间播散（spread through air spaces, STAS）的肺腺癌患者即便处于疾病最早期阶段，术后生存预后也更差且复发率更高。目前学界对STAS的分子发病机制尚不完全明确。为阐明STAS潜在的致病机制，本研究对STAS相关微阵列数据集开展了全面分析。差异表达分析显示，STAS阳性组与STAS阴性组间共鉴定出841个差异表达基因（differentially expressed genes, DEGs）。此外，本研究筛选得到2个与生存相关的核心基因。基因集变异分析（gene set variation analysis, GSVA）证实，两组间差异最为显著的信号通路为缺氧VHL靶标通路、蛋白激酶C（protein kinase C, PKC）通路以及嘧啶代谢通路。免疫活性分析结果表明，STAS阳性组中主要组织相容性复合体Ⅰ类（MHC-class-Ⅰ）分子的表达水平显著升高。本研究结果为深入理解STAS的致病机制以及发掘其用于STAS治疗的潜在治疗标志物提供了全新的视角。