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Comprehensive Identification of Bridge Genes to Explain the Progression from Chronic Hepatitis B Virus Infection to Hepatocellular Carcinoma
- Source :
- Journal of Inflammation Research
- Publication Year :
- 2021
- Publisher :
- Informa UK Limited, 2021.
-
Abstract
- Wenwei Nong,1,* Liping Ma,2,* Biyang Lan,1 Ning Liu,1 Hongzhi Yang,1 Xiaoxia Lao,2 Qiaomei Deng,2 Zhihu Huang2 1Department of General Surgery, Affiliated Minzu Hospital of Guangxi Medical University, Nanning, People’s Republic of China; 2Department of Clinical Laboratory, Affiliated Minzu Hospital of Guangxi Medical University, Nanning, People’s Republic of China*These authors contributed equally to this workCorrespondence: Zhihu HuangAffiliated Minzu Hospital of Guangxi Medical University, Nanning, People’s Republic of ChinaEmail hoftiger@126.comBackground: Hepatitis B virus infection co-occurs in 33% of individuals with hepatocellular carcinoma worldwide. However, the molecular link between hepatitis B virus and hepatocellular carcinoma is unknown. Thus, we aimed to elucidate molecular linkages underlying pathogenesis through in-depth data mining analysis.Materials and Methods: Differentially expressed genes were identified from patients with chronic hepatitis B virus infection, hepatocellular carcinoma, or both. Gene set enrichment analysis revealed signaling pathways involving differentially expressed genes. Protein-protein interaction networks, protein crosstalk, and enrichment were analyzed to determine whether differentially expressed gene products might serve as a bridge from hepatitis B virus infection to hepatocellular carcinoma pathogenesis. Prognostic potential and transcriptional and post-transcriptional regulators of bridge genes were also examined.Results: We identified vital bridge factors in hepatitis B virus infection-associated hepatocellular carcinoma. Differentially expressed genes were clustered into modules based on relative protein function. Signaling pathways associated with cancer, inflammation, immune system, and microenvironment showed significant crosstalk between modules. Thirty-two genes were dysregulated in hepatitis B virus infection-mediated hepatocellular carcinoma. CPEB3, RAB26, SLCO1B1, ST3GAL6 and XK had higher connectivity in the modular network, suggesting significant associations with survival. CDC20 and NUP107 were identified as driver genes as well as markers of poor prognosis.Conclusion: Our results suggest that the sustained inflammatory environment created by hepatitis B virus infection is a risk factor for hepatocellular carcinoma. The identification of hepatitis B virus infection-related hepatocellular carcinoma bridge genes provides testable hypotheses about the pathogenesis of hepatocellular carcinoma.Keywords: signaling pathways, molecular processes, protein-protein interactions, chronic hepatitis B virus infection, hepatocellular carcinoma
- Subjects :
- 0301 basic medicine
Immunology
protein-protein interactions
chronic hepatitis B virus infection
Biology
medicine.disease_cause
Virus
Pathogenesis
03 medical and health sciences
0302 clinical medicine
Immune system
Gene expression
medicine
Immunology and Allergy
Gene
Original Research
Hepatitis B virus
Cancer
hepatocellular carcinoma
medicine.disease
signaling pathways
molecular processes
030104 developmental biology
030220 oncology & carcinogenesis
Hepatocellular carcinoma
Cancer research
Journal of Inflammation Research
Subjects
Details
- ISSN :
- 11787031
- Volume :
- 14
- Database :
- OpenAIRE
- Journal :
- Journal of Inflammation Research
- Accession number :
- edsair.doi.dedup.....dd2af6f830fad0c601bb0f7dcd632015
- Full Text :
- https://doi.org/10.2147/jir.s298977