JAM2 是一种预后生物标志物,可抑制肺腺癌的增殖、转移和上皮-间质转化。

IF 4.3 3区 材料科学 Q1 ENGINEERING, ELECTRICAL & ELECTRONIC ACS Applied Electronic Materials Pub Date : 2024-02-25 DOI:10.1002/jgm.3679
Yanxin Dong, Jiale Zhang, Shun Xie, Shouyin Di, Boshi Fan, Taiqian Gong
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引用次数: 0

摘要

背景:交界粘附分子 2(JAM2)在包括增殖、转移和血管生成在内的各种生物学过程中发挥着关键作用,并导致肿瘤进展。尽管以往的研究强调了 JAM2 在不同癌症类型中的极化功能,但其在肺腺癌(LUAD)中的具体作用仍不清楚:在这项研究中,我们利用多个公共数据库分析了JAM2在LUAD中的表达和预后意义。利用Linkedomics数据库、Matescape数据库和R软件包,我们探索了相关基因、潜在的生物学功能以及JAM2对肿瘤微环境的影响。我们利用实时定量 PCR、Western 印迹和免疫组化进一步验证了公共数据库中的研究结果。此外,我们还进行了体外实验,以评估 JAM2 对 LUAD 细胞增殖、侵袭、迁移、凋亡和上皮-间质转化的影响。此外,我们还建立了一个异种移植模型,研究 JAM2 对肿瘤发生的体内影响:结果:我们的研究结果表明,JAM2在LUAD中明显下调,JAM2低表达的患者总生存率较低。功能富集分析表明,JAM2可能与细胞粘附、细胞外基质、细胞连接和增殖调控等过程有关。值得注意的是,JAM2表达的增加与较高的肿瘤微环境评分和较低的免疫细胞丰度相关。此外,JAM2 的过表达可诱导细胞凋亡,抑制肿瘤增殖,并通过调节上皮-间质转化对肿瘤的侵袭和迁移产生潜在的抑制作用。此外,体内实验证实,JAM2 的过表达会导致肿瘤生长的减少:总之,我们的研究强调了 JAM2 低表达作为 LUAD 患者不良预后预测因子的临床意义。此外,研究还发现 JAM2 对肿瘤进展的各个方面都有抑制作用。因此,JAM2有望成为LUAD患者的预后生物标志物和潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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JAM2 is a prognostic biomarker and inhibits proliferation, metastasis and epithelial–mesenchymal transition in lung adenocarcinoma

Background

Junctional adhesion molecule 2 (JAM2) plays a pivotal role in various biological processes, including proliferation, metastasis and angiogenesis, contributing to tumor progression. While previous studies have highlighted the polarizing functions of JAM2 in different cancer types, its specific role in lung adenocarcinoma (LUAD) remains unclear.

Methods

In this study, we harnessed multiple public databases to analyze the expression and prognostic significance of JAM2 in LUAD. Using the Linkedomics database, Matescape database and R package, we explored the associated genes, the potential biological functions and the impact of JAM2 on the tumor microenvironment. Our findings from public databases were further validated using real-time quantitative PCR, western blot and immunohistochemistry. Additionally, in vitro experiments were conducted to assess the influence of JAM2 on LUAD cell proliferation, invasion, migration, apoptosis and epithelial–mesenchymal transition. Furthermore, we established a xenograft model to investigate the in vivo effects of JAM2 on tumorigenesis.

Results

Our results revealed a significant downregulation of JAM2 in LUAD, and patients with low JAM2 expression exhibited unfavorable overall survival outcomes. Functional enrichment analysis indicated that JAM2 may be associated with processes such as cell adhesion, extracellular matrix, cell junctions and regulation of proliferation. Notably, increased JAM2 expression correlated with higher tumor microenvironment scores and reduced immune cell abundance. Furthermore, overexpression of JAM2 induced apoptosis, suppressed tumor proliferation and exhibited potential inhibitory effects on tumor invasion and migration through the modulation of epithelial–mesenchymal transition. Additionally, in vivo experiments confirmed that JAM2 overexpression led to a reduction in tumor growth.

Conclusion

Overall, our study highlights the clinical significance of low JAM2 expression as a predictor of poor prognosis in LUAD patients. Moreover, JAM2 was found to exert inhibitory effects on various aspects of tumor progression. Consequently, JAM2 emerges as a promising prognostic biomarker and a potential therapeutic target for LUAD patients.

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CiteScore
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自引率
4.30%
发文量
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