IRF5 promotes glycolysis in the progression of hepatocellular carcinoma and is regulated by TRIM35

ObjectivesThe interferon regulatory factor (IRF) family of proteins are involved in tumor progression. However, the role of IRF5 in tumorigenesis remains unknown. In this study we aimed to elucidate the functions of IRF5 in the progression of hepatocellular carcinoma (HCC).MethodsIRF5 expression in...

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Published in:Journal of digestive diseases 2023-08, Vol.24 (8-9), p.480-490
Main Authors: Fang, Ying, Lu, Zhi Hui, Liu, Bang Zhong, Li, Nan, Yang, Ming Zhen, Wang, Ping
Format: Article
Language:English
Subjects:
Cell proliferation
Glycolysis
Hepatocellular carcinoma
Immunohistochemistry
Immunoprecipitation
Interferon regulatory factor
L-Lactate dehydrogenase
Liver cancer
Molecular modelling
Tumorigenesis
Ubiquitination
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Summary:ObjectivesThe interferon regulatory factor (IRF) family of proteins are involved in tumor progression. However, the role of IRF5 in tumorigenesis remains unknown. In this study we aimed to elucidate the functions of IRF5 in the progression of hepatocellular carcinoma (HCC).MethodsIRF5 expression in HCC was analyzed through quantitative polymerase chain reaction (qPCR), western blot, and immunohistochemistry (IHC), etc. The Cell Counting Kit 8 (CCK8) assay, anchorage‐independent assay, and EdU assay were used to evaluate the role of IRF5. The molecular mechanisms were studied by analyzing the metabolites with mass spectrum and immunoprecipitation.ResultsIRF5 was upregulated in HCC. Interfering with IRF5 inhibited the proliferation and tumorigenic potential of HCC cells. When studying the molecular mechanism, IRF5 was found to upregulate the expression of lactate dehydrogenase A (LDHA) and promoted glycolysis. Additionally, tripartite motif containing 35 (TRIM35) interacted with IRF5, promoting its ubiquitination and degradation. In the clinically obtained HCC samples, TRIM35 was negatively correlated with the expression of IRF5.ConclusionThese findings reveal the oncogenic function of IRF5 in the progression of HCC by enhancing glycolysis, further supporting the potential of IRF5 as a viable target for HCC therapy.
ISSN:1751-2972
1751-2980
DOI:10.1111/1751-2980.13218