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TREM2 作为皮肤黑色素瘤微环境中患者预后的潜在免疫相关生物标志物。

TREM2 as a Potential Immune-Related Biomarker of Prognosis in Patients with Skin Cutaneous Melanoma Microenvironment.

机构信息

Department of Dermatology, Shanghai Key Laboratory of Medical Mycology, Changzheng Hospital, Naval Medical University, Shanghai, China.

Department of Vascular Surgery, Changhai Hospital, Naval Medical University, Shanghai, China.

出版信息

Dis Markers. 2023 Jan 27;2023:8101837. doi: 10.1155/2023/8101837. eCollection 2023.

DOI:10.1155/2023/8101837
PMID:36741909
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9897921/
Abstract

BACKGROUND

The skin cutaneous melanoma (SKCM) is a devastating form of skin cancer triggered by genetic and environmental factors, and the incidence of SKCM has rapidly increased in recent years. Immune infiltration of the tumor microenvironment is positively associated with overall survival in many tumors. Triggering receptor expressed on myeloid cells 2 (TREM2) is a transmembrane receptor of the immunoglobulin superfamily and a crucial signaling hub for multiple pathological pathways that mediate immunity. Although numerous evidences suggest a crucial role for TREM2 in tumorigenesis of some tumors, no systematic SKCM analysis of TREM2 is available. . The relationship between TREM2 expression and diagnostic and prognostic value of SKCM patients via using The Cancer Genome Atlas (TCGA) data. The expression level of TREM2 and clinical characteristic correlation in SKCM patients were assessed by the Wilcoxon rank sum test. The cox regression methods, Kaplan-Meier (KM), and log-rank test were used to assess the impact of TREM2 expression on the overall survival (OS). Furthermore, the Gene Set Enrichment Analysis (GSEA) and TIMER were performed to evaluate the enrichment pathways and potential functions and quantify the immune cell infiltration level for TREM2 expression.

RESULTS

The TREM2 in SKCM sample expression levels was significantly higher than in normal tissues. Moreover, this expression level of TREM2 was also associated with the BMI of SKCM patients. KM overall survival analysis and OS curve displayed that a high-level TREM2 expression was significantly correlated with a better SKCM prognosis of patients as compared with a low level of TREM2 expression. The GSEA analysis also revealed that TREM2 was associated with immune functions, such as neutrophil activation.

CONCLUSION

TREM2 played a crucial role in SKCM, which might be a prognostic biomarker and correlated with immune infifiltrates in SKCM patients.

摘要

背景

皮肤黑色素瘤(SKCM)是一种由遗传和环境因素引发的毁灭性皮肤癌,近年来 SKCM 的发病率迅速上升。肿瘤微环境中的免疫浸润与许多肿瘤的总生存率呈正相关。髓样细胞触发受体 2(TREM2)是免疫球蛋白超家族的跨膜受体,是介导免疫的多个病理途径的关键信号枢纽。尽管有大量证据表明 TREM2 在一些肿瘤的肿瘤发生中起着至关重要的作用,但目前尚无针对 SKCM 的 TREM2 的系统分析。本研究旨在通过分析 TCGA 数据,探讨 TREM2 在 SKCM 中的表达及其与 SKCM 患者诊断和预后的关系。采用 Wilcoxon 秩和检验评估 TREM2 在 SKCM 患者中的表达水平与临床特征的相关性。采用 Cox 回归方法、Kaplan-Meier(KM)和对数秩检验评估 TREM2 表达对总生存率(OS)的影响。此外,还进行了基因集富集分析(GSEA)和 TIMER,以评估 TREM2 表达的富集途径和潜在功能,并量化 TREM2 表达的免疫细胞浸润水平。

结果

TREM2 在 SKCM 样本中的表达水平明显高于正常组织。此外,TREM2 的这种表达水平也与 SKCM 患者的 BMI 相关。KM 总体生存分析和 OS 曲线显示,与低水平的 TREM2 表达相比,高水平的 TREM2 表达与 SKCM 患者更好的预后显著相关。GSEA 分析还表明,TREM2 与免疫功能相关,如中性粒细胞激活。

结论

TREM2 在 SKCM 中发挥着关键作用,可能是一种预后生物标志物,并与 SKCM 患者的免疫浸润相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/e3f6b55a3430/DM2023-8101837.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/15b207146858/DM2023-8101837.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/97c2adb130e9/DM2023-8101837.005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/e3f6b55a3430/DM2023-8101837.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/15b207146858/DM2023-8101837.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/b6205defda7f/DM2023-8101837.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/12466d36b62f/DM2023-8101837.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/6cac7402a810/DM2023-8101837.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/97c2adb130e9/DM2023-8101837.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/c3a6d26eeb2a/DM2023-8101837.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/40edfc3260b8/DM2023-8101837.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da1c/9897921/e3f6b55a3430/DM2023-8101837.008.jpg

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Blockade of the co-inhibitory molecule PD-1 unleashes ILC2-dependent antitumor immunity in melanoma.
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