Joint Analysis of CCAAT/Enhancer-Binding Protein Beta and Interleukin 1 Beta in the Treatment and Prognosis of Diffuse Large B-Cell Lymphoma

Autor: Hongmin Wang, Shuo Zhang, Mengmeng Wang, Chaozhong Wang, Jihong Xu, Ming Jiang, Xue Han, Xiaotong Yang, Liping Zhang, Baotong Chen, Aichun Liu
Jazyk: angličtina
Rok vydání: 2024
Předmět:
Zdroj: Frontiers in Bioscience-Landmark, Vol 29, Iss 11, p 372 (2024)
Druh dokumentu: article
ISSN: 2768-6701
DOI: 10.31083/j.fbl2911372
Popis: Objective: The purpose of this study is to investigate the correlation between elevated levels of CCAAT/enhancer-binding protein beta (CEBPB) gene expression and unfavorable outcomes in diffuse large B-cell lymphoma (DLBCL). The goal is to elucidate potential therapeutic targets associated with this relationship. Methods: Differential expression and survival analyses were conducted using data from the Gene Expression Omnibus (GEO) database. The functions of CEBPB in DLBCL cells were investigated through cell culture, RNA extraction, quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot. In addition, a weighted gene co-expression network analysis (WGCNA) was performed to pinpoint gene modules associated with CEBPB. Furthermore, experimental validation was carried out to explore the interaction between CEBPB and interleukin 1 beta (IL1B). Results: High levels of CEBPB expression are prominently observed in DLBCL, with its overabundance significantly linked to the diagnosis of DLBCL. Survival analysis reveals that patients exhibiting elevated CEBPB expression tend to experience a poorer prognosis. Further validation confirmed CEBPB's role in promoting DLBCL cell proliferation and cell cycle progression. WGCNA identified CEBPB-related gene modules, with IL1B identified as a potential regulatory gene of CEBPB. The presence of high levels of IL1B has been correlated with an unfavorable prognosis in individuals diagnosed with DLBCL. Experiments demonstrate that IL1B promotes DLBCL cell proliferation through CEBPB. Conclusions: This study reveals the significant roles of CEBPB and IL1B in DLBCL, providing new theoretical foundations and potential molecular targets for the treatment and prognosis of DLBCL.
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