RESEARCH ARTICLE
CLEC4A Expression as a Prognostic Biomarker and Immunoregulator in Lung Adenocarcinoma: Insights from Immune Cell Infiltration
Huiyun Ma1, 2, #, Gujie Wu1, #, Hongyu Chen1, #, Qin Hu1, Zhouwei Zhang1, Fei Wang1, *, Qun Xue1, *
Article Information
Identifiers and Pagination:
Year: 2024Volume: 11
E-location ID: e18742203270381
Publisher ID: e18742203270381
DOI: 10.2174/0118742203270381240209060006
Article History:
Received Date: 25/09/2023Revision Received Date: 15/02/2024
Acceptance Date: 15/02/2024
Electronic publication date: 18/4/2024
Collection year: 2024
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background
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.
Methods
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.
Results
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.
Conclusion
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.
