SGO2是一种与肺腺癌细胞增殖、迁移、侵袭和上皮-间质转化相关的预后生物标志物

IF 3.3 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yinghua Chen, Tingxiu Xiang
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引用次数: 0

摘要

背景:肺腺癌(LUAD)是非小细胞肺癌病例中最主要的组织学亚型,约占所有病例的 40%。舒戈欣 2 (SGO2) 与肿瘤发生和进展有关。本研究旨在揭示SGO2在LUAD中的潜在作用:基因 mRNA 表达相关数据和临床信息来自癌症基因组图谱(TCGA)、基因型-组织表达(GTEx)和癌症细胞系百科全书(CCLE)数据库。应用细胞计数试剂盒-8(CCK-8)、Transwell、划痕试验和流式细胞术研究 SGO2 在 LUAD 中的生物学功能。结果显示,通过泛癌分析,SGO2在LUAD中的表达量明显高于SGO2:结果:通过泛癌分析发现,在 33 种癌症类型中,SGO2 在 25 种类型中持续过表达,其中包括 LUAD。体外实验显示,SGO2敲除会显著阻碍细胞增殖、细胞迁移、侵袭和上皮-间质转化(EMT),而过表达则会促进这些能力。流式细胞术证实,SGO2 促进了细胞周期的进展并减少了细胞凋亡。此外,SGO2 通过上调重组 E2F 转录因子 1(E2F1)促进细胞增殖并调节细胞周期:我们的研究表明,SGO2在包括LUAD在内的泛癌中上调,其高表达与LUAD患者的总生存期(OS)和无进展生存期(PFS)差密切相关。SGO2 促进了 A549 细胞的增殖、细胞迁移、侵袭和 EMT。此外,E2F1参与了SGO2介导的细胞周期和细胞增殖调控。这项研究阐明了SGO2在LUAD中的致癌意义,提出了其作为预后生物标志物和治疗干预靶点的潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
SGO2 as a Prognostic Biomarker Correlated with Cell Proliferation, Migration, Invasion, and Epithelial-Mesenchymal Transition in Lung Adenocarcinoma.

Background: Lung adenocarcinoma (LUAD) is the predominant histological subtype among non-small cell lung cancer cases, representing approximately 40% of all cases. Shugoshin 2 (SGO2) is implicated in tumorigenesis and tumor progression. This study aimed to uncover a potential role of SGO2 in the LUAD.

Methods: Data related to gene mRNA expression and clinical information were obtained from The Cancer Genome Atlas (TCGA), The Genotype-Tissue Expression (GTEx), and the Cancer Cell Line Encyclopedia (CCLE) databases. Cell Counting Kit-8 (CCK-8), Transwell, scratch assay, and flow cytometry were applied to investigate the biological functions of SGO2 in the LUAD. Western blot was conducted to detect the protein expression.

Results: Through pan-cancer analysis, SGO2 was found to be consistently overexpressed in 25 of 33 cancer types, including LUAD. In vitro assays revealed that SGO2 knockdown significantly impeded cell proliferation, cell migration, invasion and epithelial-mesenchymal transition (EMT), whereas its overexpression promoted these abilities. Flow cytometry confirmed that SGO2 contributed to cell cycle progression and reduced cell apoptosis. Furthermore, SGO2 facilitated cell proliferation and regulated cell cycle through upregulating recombinant E2F transcription factor 1 (E2F1).

Conclusions: Our study demonstrated that SGO2 was up-regulated in pan-cancers including LUAD and its high expression was strongly associated with poor overall survival (OS) and progression-free survival (PFS) of patients with LUAD. SGO2 promoted cell proliferation, cell migration, invasion and EMT of A549 cells. Additionally, E2F1 was involved in regulation of cell cycle and cell proliferation mediated by SGO2. This research elucidated the oncogenic significance of SGO2 in LUAD, proposing its potential as a prognostic biomarker and a promising target for therapeutic interventions.

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