ArticleOncotarget2016
HBx regulates fatty acid oxidation to promote hepatocellular carcinoma survival during metabolic stress.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 74 citations in OpenAlex.
- Review
- Metabolic hijackers: how viral proteins redefine host cell landscapes.Journal of virology · 2026Review
- HBV and host metabolic crosstalk: Reprogramming pathways for viral replication and pathogenesis.Virologica Sinica · 2025Review
- Emerging roles for fatty acid oxidation in cancer.Genes & diseases · 2025Review
- From genes to therapy: a lipid Metabolism-Related genetic risk model predicts HCC outcomes and enhances immunotherapy.BMC cancer · 2025Article
- Metabolic reprogramming and interventions in angiogenesis.Journal of advanced research · 2025Review
- Modulation of lipid metabolism by exercise: exploring its potential as a therapeutic target in cancer endocrinology.Frontiers in endocrinology · 2025Review
- The novel mechanism facilitating chronic hepatitis B infection: immunometabolism and epigenetic modification reprogramming.Frontiers in immunology · 2024Review
- Enhancing prognostic accuracy in head and neck squamous cell carcinoma chemotherapy via a lipid metabolism-related clustered polygenic model.Cancer cell international · 2023Article
- [Analysis of clinical and pathological features of chronic hepatitis B combined with metabolic-associated fatty liver disease].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2023Article
- The Ketogenic Diet in Colorectal Cancer: A Means to an End.International journal of molecular sciences · 2023Review
- The crosstalk among the physical tumor microenvironment and the effects of glucose deprivation on tumors in the past decade.Frontiers in cell and developmental biology · 2023Review
- Review
- The role of liver kinase B1 in tumor progression through regulation of lipid metabolism.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2022Review
- Transcriptomic Analysis of Livers of Inactive Carriers of Hepatitis B Virus With Distinct Expression of Hepatitis B Surface Antigen.The Journal of infectious diseases · 2022Article
- Signaling Induced by Chronic Viral Hepatitis: Dependence and Consequences.International journal of molecular sciences · 2022Review
- CaMicroorganisms · 2022Article
- Tumor Glucose and Fatty Acid Metabolism in the Context of Anthracycline and Taxane-Based (Neo)Adjuvant Chemotherapy in Breast Carcinomas.Frontiers in oncology · 2022Review
- Perspectives of lipid metabolism reprogramming in head and neck squamous cell carcinoma: An overview.Frontiers in oncology · 2022Review
- What role for cellular metabolism in the control of hepatitis viruses?Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Due to a high rate of nutrient consumption and inadequate vascularization, hepatocellular carcinoma (HCC) cells constantly undergo metabolic stress during tumor development. Hepatitis B virus (HBV) X protein (HBx) has been implicated in the pathogenesis of HBV-induced HCC. In this study, we investigated the functional roles of HBx in HCC adaptation to metabolic stress. Up-regulation of HBx increased the intracellular ATP and NADPH generation, and induced the resistance to glucose deprivation, whereas depletion of HBx via siRNA abolished these effects and conferred HCC cells sensitive to glucose restriction. Though HBx did not affect the glycolysis and oxidative phosphorylation capacity of HCC cells under normal culture conditions, it facilitated fatty acid oxidation (FAO) in the absence of glucose, which maintained NADPH and ATP levels. Further investigation showed that HBx expression, under glucose deprivation, stimulated phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) via a calcium/CaMKK-dependent pathway, which was required for the activation of FAO. Conversely, inhibition of FAO by etomoxir (ETO) restored the sensitivity of HBx-expressing cells to glucose deficiency in vitro and retarded xenograft tumor formation in vivo. Finally, HBx-induced activation of the AMPK and FAO pathways were also observed in xenograft tumors and HBV-associated HCC specimens. Our data suggest that HBx plays a key role in the maintenance of redox and energy homeostasis by activating FAO, which is critical for HCC cell survival under conditions of metabolic stress and might be exploited for therapeutic benefit.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.