Zeng Yuan, Zhou Lingli, Jia Dexin, Pan Bo, Li Xiaomei, Yu Yan
Department of Medical Oncology, Harbin Medical University Cancer Hospital, Harbin, China.
Department of Respiratory Medicine, Suizhou Hospital, Hubei University of Medicine, Hubei, China.
Front Genet. 2022 Aug 22;13:900864. doi: 10.3389/fgene.2022.900864. eCollection 2022.
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.
在肺腺癌中，存在气腔播散（STAS）的患者术后生存率较低且复发率较高，即便在疾病的最早期阶段亦是如此。目前，STAS的分子发病机制尚未完全明确。因此，为阐明STAS的潜在致病机制，我们对一个STAS微阵列数据集进行了全面分析。差异表达分析显示，STAS阳性组和STAS阴性组之间有841个差异表达基因（DEG）。此外，我们获得了两个与生存相关的枢纽基因。基因集变异分析（GSVA）证实，两组之间主要的差异信号通路为缺氧VHL靶点、蛋白激酶C（PKC）和嘧啶代谢通路。免疫活性分析表明，STAS阳性组中观察到MHC-Ⅰ类分子的表达增加。这些发现为更好地了解STAS的致病机制以及STAS治疗的潜在治疗标志物提供了新的见解。
