IRF5 promotes the glycolysis in the progression of hepatocellular carcinoma and is regulated by TRIM35
Ying Fang, Zhi Hui Lu, Bang Zhong Liu, Nan Li, Ming Zhen Yang, Ping Wang - Gastroenterology
Abstract
Background
The IRF family of proteins involves in the tumor progression. However, the functions of IRF5 in the tumorigenesis are largely unknown.
Methods
The levels of IRF5 were analyzed through various techniques including qPCR, western blot and immunohistochemistry (IHC) in the hepatocellular carcinoma (HCC). The 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.
Results
Here, IRF5 was observed to be up regulated in hepatocellular carcinoma (HCC). Interfering with IRF5 inhibited the proliferation and tumorigenic potential of HCC cells. When studying the molecular mechanism, IRF5 was found to up‐regulate the expression of LDHA and promoted glycolysis. Additionally, it was found that TRIM35 interacted with IRF5, promoting the ubiquitination and degradation of IRF5. In the clinical specimens of HCC, TRIM35 was negatively correlated with the expression of IRF5.
Conclusions
These observations 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.
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