The Role of FCRLB in Predicting Thyroid Cancer Prognosis and Regulating Thyroid Cancer Cell Proliferation and Apoptosis

Bo Yu, Jiaxing Yao, Weiye Fan, Chenlei Shi, Songpu Li, Fulin Dou, Xiyuan Sun, Ning Xu

Article ID: 7931
Vol 38, Issue 3, 2024
DOI: https://doi.org/10.23812/j.biol.regul.homeost.agents.20243803.199
Received: 20 March 2024; Accepted: 20 March 2024; Available online: 20 March 2024; Issue release: 20 March 2024

Abstract

Background: Immunogenic cell death (ICD)-related gene signatures demonstrate prognostic significance across multiple cancer types. Nevertheless, the differential expression of these genes in thyroid carcinoma (THCA) and their application in predicting the survival outcomes of individuals with THCA remain poorly understood. Therefore, this study aimed to explore the role of ICD-related genes in predicting the survival outcomes of THCA patients. Methods: The expression of ICD-related genes was analyzed using RNA-seq data and compared with clinicopathological features from The Cancer Genome Atlas-thyroid carcinoma cohort. The role of Fc receptor-like B (FCRLB) in thyroid cancer was identified using Methyl Thiazolyl Tetrazolium (MTT) assay, 7-amino-actinomycin D staining, and Annexin V-fluorescein isothiocyanate staining assay. Results: We identified FCRLB as a novel marker for predicting THCA survival. Moreover, bioinformatic analyses revealed a significant correlation between elevated FCRLB expression and increased levels of immune infiltration and somatic mutations, potentially contributing to a poorer prognosis in THCA (p < 0.05). Furthermore, we observed overexpression of FCRLB in THCA cells compared to thyroid epithelial cells (p < 0.05). Additionally, reduced proliferation, cell cycle arrest, and enhanced apoptosis were the outcomes of FCRLB knockdown in TPC-1 THCA cells (p < 0.05). Conclusions: These findings suggest that FCRLB overexpression predicts poor THCA survival and might contribute to THCA development.


Keywords

immunogenic cell death;Fc receptor-like B;tumor immune infiltration;knockdown;cell proliferation


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