作为肺腺癌预后生物标记物和免疫调节因子的 CLEC4A 表达:免疫细胞浸润的启示

Huiyun Ma, Gujie Wu, Hongyu Chen, Qin Hu, Zhouwei Zhang, Fei Wang, Qun Xue
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引用次数: 0

摘要

CLEC4A(C-型凝集素结构域4家族成员A)是C-型(Ca2+依赖性)凝集素(CLEC)受体的一个成员,是树突状细胞(DC)的免疫抑制剂,在先天性免疫和适应性免疫中发挥着重要作用,但它在肺腺癌(LUAD)中的作用及其免疫治疗的潜力仍有待研究。 为了实现我们的目标,我们对 CLEC4A 的表达及其与 LUAD 临床因素的相关性进行了全面分析。我们利用公开的数据集,如癌症基因组图谱(TCGA)和其他相关资源,收集了LUAD患者的基因表达和临床数据。此外,我们还研究了CLEC4A表达水平与肺腺癌临床病理分期和预后的关系。我们利用 TIMER 数据库分析了免疫细胞浸润情况,而 TISIDB 数据库则提供了淋巴细胞浸润和免疫调节因子的相关信息。 我们的分析表明,LUAD 患者预后不良与 CLEC4A 低表达之间存在显著相关性。CLEC4A 的低表达与不良临床因素相关,这表明它有可能成为 LUAD 的预后生物标志物。此外,我们还观察到 CLEC4A 表达与免疫细胞浸润之间存在值得注意的关系。CLEC4A 表达的增加与肿瘤微环境中 CD8+ T 细胞、CD4+ T 细胞、树突状细胞(DC)和 B 细胞浸润水平的升高相关。这表明,CLEC4A 在调节针对 LUAD 的免疫反应中发挥着免疫调节作用。此外,我们的分析还强调了 CLEC4A 表达与淋巴细胞存在之间的正相关性,这进一步强调了 CLEC4A 在肿瘤免疫中的潜在重要性。此外,对免疫相关因素的调查表明,CLEC4A 可能参与了肿瘤微环境中的免疫调节。 这项研究为CLEC4A在肺腺癌(LUAD)中的表达、预后和潜在免疫治疗作用提供了宝贵的见解。CLEC4A 的表达与临床特征、免疫细胞浸润和淋巴细胞浸润之间的相关性凸显了 CLEC4A 作为 LUAD 潜在生物标记物和治疗靶点的重要性。为了阐明 LUAD 的潜在机制并利用针对 CLEC4A 的治疗潜力,有必要开展进一步的研究。这些努力将有助于改善 LUAD 患者的预后。
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CLEC4A Expression as a Prognostic Biomarker and Immunoregulator in Lung Adenocarcinoma: Insights from Immune Cell Infiltration
CLEC4A (C-type lectin domain family 4 member A), a member of the C-type (Ca2+-dependent) lectin (CLEC) receptor, is an immunosuppressant of dendritic cells (DCs) and plays an important role in innate and adaptive immunity, however, its role in lung adenocarcinoma (LUAD) and the potential for immunotherapy remains to be investigated. To achieve our objectives, we conducted a comprehensive analysis of CLEC4A expression and its correlation with clinical factors in LUAD. We utilized publicly available datasets, such as The Cancer Genome Atlas (TCGA) and other relevant resources, to gather gene expression and clinical data from LUAD patients. Furthermore, we investigated the association of CLEC4A expression levels with clinical pathological staging and prognosis of lung adenocarcinoma. The TIMER database was utilized to analyze immune cell infiltration, while the TISIDB database provided insights into lymphocyte infiltration and immune regulatory factors. Our analysis revealed a significant correlation between poor prognosis and low CLEC4A expression in LUAD patients. Reduced expression of CLEC4A was associated with adverse clinical factors, indicating its potential as a prognostic biomarker in LUAD. Moreover, we observed a noteworthy relationship between CLEC4A expression and immune cell infiltration. Increased CLEC4A expression was correlated with higher infiltration levels of CD8+ T cells, CD4+ T cells, dendritic cells (DC), and B cells within the tumor microenvironment. This indicates an immunoregulatory role for CLEC4A in modulating immune responses against LUAD. Additionally, our analysis highlighted a positive correlation between CLEC4A expression and the presence of lymphocytes, further emphasizing its potential importance in tumor immunity. Furthermore, the investigation of immune-related factors indicated a potential involvement of CLEC4A in immune regulation within the tumor microenvironment. This study provides valuable insights into the expression, prognosis, and potential immunotherapeutic role of CLEC4A in lung adenocarcinoma (LUAD). The identified correlations between CLEC4A expression and clinical characteristics, immune cell infiltration, and lymphocyte infiltration highlight the significance of CLEC4A as a potential biomarker and therapeutic target for LUAD. Further research is warranted to elucidate the underlying mechanisms and capitalize on the therapeutic potential of targeting CLEC4A in LUAD. These efforts could contribute to improving patient outcomes and prognosis in LUAD.
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