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BTN3A2表达与肺腺癌的良好预后及高浸润性免疫相关。

BTN3A2 Expression Is Connected With Favorable Prognosis and High Infiltrating Immune in Lung Adenocarcinoma.

作者信息

Lin Yuansheng, Zhou Hao, Li Shengjun

机构信息

Suzhou Science and Technology Town Hospital, Gusu School, Nanjing Medical University, Suzhou, China.

出版信息

Front Genet. 2022 Jul 6;13:848476. doi: 10.3389/fgene.2022.848476. eCollection 2022.

DOI:10.3389/fgene.2022.848476
PMID:35873496
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9298880/
Abstract

Butyrophilin subfamily 3 member A2 (BTN3A2) is an important mediator in immune activation, and it is reported to be linked to many cancer progresses. However, the relation with infiltrating immune and prognosis of BTN3A2 in lung adenocarcinoma are not clear. In our study, we checked the mRNA expression and protein expression profile of BTN3A2 in lung adenocarcinoma (LUAD) and its relation to clinical outcomes using TIMER and UALCAN databases. In addition, we analyzed the survival of BTN3A2 in LUAD using the Kaplan-Meier Plotter database and PrognoScan database. Moreover, we analyzed gene set enrichment analysis (GSEA) of the BTN3A2. Next, we explored the relation of BTN3A2 expression with the immune infiltration by TIMER. At last, in order to enrich the regulatory mechanism of BTN3A2, we used miRarbase, starbase, and miRDB databases to look for miRNA targets of BTN3A2. The mRNA along with the protein expression of BTN3A2 in the LUAD group was lower than that in the normal group. In addition, high BTN3A2 expression was connected with good first progression (FP) and overall survival (OS) in LUAD. Then, the GSEA analysis demonstrated that T-cell receptor signaling cascade, B-cell receptor signaling cascade, natural killer cell-mediated cytotoxicity, immune receptor activity, immunological synapse, and T-cell activation were enriched differentially in the BTN3A2 high expression phenotype of LUAD. Moreover, BTN3A2 expression is a remarkable positive correlation with invading levels of tumor purity, B cells, neutrophils, CD4+ T cells, dendritic cells, macrophages, and CD8+ T cells in LUAD, and B cells and dendritic cells were linked with a good prognosis of LUAD. To further enrich the possible regulatory mechanisms of BTN3A2, we analyzed the miRNA targets. The results showed that hsa-miR-17-5p may be miRNA targets of BTN3A2. Taking together, we provide evidence of BTN3A2 as possible prognosis biomarkers of LUAD. In addition, high BTN3A2 expression in LUAD may influence the prognosis because of immune invasion. Moreover, our findings provide a potential mechanism that hsa-miR-17-5p may be miRNA targets of BTN3A2.

摘要

嗜乳脂蛋白亚家族3成员A2(BTN3A2)是免疫激活中的重要介质,据报道它与许多癌症进展相关。然而,BTN3A2在肺腺癌中的浸润性免疫及预后关系尚不清楚。在我们的研究中,我们使用TIMER和UALCAN数据库检查了BTN3A2在肺腺癌(LUAD)中的mRNA表达和蛋白质表达谱及其与临床结果的关系。此外,我们使用Kaplan-Meier Plotter数据库和PrognoScan数据库分析了BTN3A2在LUAD中的生存情况。此外,我们对BTN3A2进行了基因集富集分析(GSEA)。接下来,我们通过TIMER探讨了BTN3A2表达与免疫浸润的关系。最后,为了丰富BTN3A2的调控机制,我们使用miRarbase、starbase和miRDB数据库寻找BTN3A2的miRNA靶点。LUAD组中BTN3A2的mRNA及蛋白质表达均低于正常组。此外,高BTN3A2表达与LUAD的良好首次进展(FP)和总生存期(OS)相关。然后,GSEA分析表明,在LUAD的BTN3A2高表达表型中,T细胞受体信号级联、B细胞受体信号级联、自然杀伤细胞介导的细胞毒性、免疫受体活性、免疫突触和T细胞激活存在差异富集。此外,BTN3A2表达与LUAD中肿瘤纯度、B细胞、中性粒细胞、CD4+T细胞、树突状细胞、巨噬细胞和CD8+T细胞的浸润水平呈显著正相关,且B细胞和树突状细胞与LUAD的良好预后相关。为了进一步丰富BTN3A2可能的调控机制,我们分析了miRNA靶点。结果表明,hsa-miR-17-5p可能是BTN3A2的miRNA靶点。综上所述,我们提供了BTN3A2作为LUAD可能的预后生物标志物的证据。此外,LUAD中高BTN3A2表达可能由于免疫浸润而影响预后。此外,我们的研究结果提供了一种潜在机制,即hsa-miR-17-5p可能是BTN3A2的miRNA靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/cfe2b8c72e6b/fgene-13-848476-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/ac91f8f316f5/fgene-13-848476-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/b3e59412f1f8/fgene-13-848476-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/32517e0bf94f/fgene-13-848476-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/cfe2b8c72e6b/fgene-13-848476-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/ac91f8f316f5/fgene-13-848476-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/7298df2f7205/fgene-13-848476-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/b6c311a9e12b/fgene-13-848476-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/75d6440583c7/fgene-13-848476-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/b3e59412f1f8/fgene-13-848476-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/32517e0bf94f/fgene-13-848476-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3974/9298880/cfe2b8c72e6b/fgene-13-848476-g007.jpg

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