Chemerin Is Induced in Non-Alcoholic Fatty Liver Disease and Hepatitis B-Related Hepatocellular Carcinoma

Haberl, Elisabeth M.; Feder, Susanne; Pohl, Rebekka; Rein-Fischboeck, Lisa; Dürholz, Kerstin; Eichelberger, Laura; Wanninger, Josef; Weiss, Thomas S.; Buechler, Christa

doi:10.3390/cancers12102967

Cited by 16 publications

(16 citation statements)

References 42 publications

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“…Many studies in rodent models indicate that chemokines play a crucial role in NAFLD. 28,29 The levels of CCL20 were increased in the animal models of liver injury, especially with the acute-on-chronic condition. 30 Results from a network meta-analysis showed that the concentrations of chemokines, including CCL20, in the NASH group were higher than those in the control group.…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes and pathways in mild and severe nonalcoholic fatty liver disease by integrative analysis

Feng

Wei

Cui

et al. 2021

Chronic Diseases and Translational Medicine

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Background The global prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing. The pathogenesis of NAFLD is multifaceted, and the underlying mechanisms are elusive. We conducted data mining analysis to gain a better insight into the disease and to identify the hub genes associated with the progression of NAFLD. Methods The dataset GSE49541, containing the profile of 40 samples representing mild stages of NAFLD and 32 samples representing advanced stages of NAFLD, was acquired from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) were identified using the R programming language. The Database for Annotation, Visualization and Integrated Discovery (DAVID) online tool and Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) database were used to perform the enrichment analysis and construct protein–protein interaction (PPI) networks, respectively. Subsequently, transcription factor networks and key modules were identified. The hub genes were validated in a mice model of high fat diet (HFD)-induced NAFLD and in cultured HepG2 cells by real-time quantitative PCR. Results Based on the GSE49541 dataset, 57 DEGs were selected and enriched in chemokine activity and cellular component, including the extracellular region. Twelve transcription factors associated with DEGs were indicated from PPI analysis. Upregulated expression of five hub genes ( SOX9 , CCL20 , CXCL1 , CD24 , and CHST4 ), which were identified from the dataset, was also observed in the livers of HFD-induced NAFLD mice and in HepG2 cells exposed to palmitic acid or advanced glycation end products. Conclusion The hub genes SOX9 , CCL20 , CXCL1 , CD24 , and CHST4 are involved in the aggravation of NAFLD. Our results offer new insights into the underlying mechanism of NAFLD progression.

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Section: Discussionmentioning

confidence: 99%

Identification of key genes and pathways in mild and severe nonalcoholic fatty liver disease by integrative analysis

Feng

Wei

Cui

et al. 2021

Chronic Diseases and Translational Medicine

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“…The characteristics of the participants were summarized in Table 3 . Tissues of patients with viral infections were used in a previous study to measure chemerin and CMKLR1 in the liver tissues [ 62 ].…”

Section: Methodsmentioning

confidence: 99%

Liver Lipids of Patients with Hepatitis B and C and Associated Hepatocellular Carcinoma

Haberl

Weiss

Peschel

et al. 2021

IJMS

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Hepatocellular carcinoma (HCC) still remains a difficult to cure malignancy. In recent years, the focus has shifted to lipid metabolism for the treatment of HCC. Very little is known about hepatitis B virus (HBV) and C virus (HCV)-related hepatic lipid disturbances in non-malignant and cancer tissues. The present study showed that triacylglycerol and cholesterol concentrations were similar in tumor adjacent HBV and HCV liver, and were not induced in the HCC tissues. Higher levels of free cholesterol, polyunsaturated phospholipids and diacylglycerol species were noted in non-tumorous HBV compared to HCV liver. Moreover, polyunsaturated phospholipids and diacylglycerols, and ceramides declined in tumors of HBV infected patients. All of these lipids remained unchanged in HCV-related HCC. In HCV tumors, polyunsaturated phosphatidylinositol levels were even induced. There were no associations of these lipid classes in non-tumor tissues with hepatic inflammation and fibrosis scores. Moreover, these lipids did not correlate with tumor grade or T-stage in HCC tissues. Lipid reprogramming of the three analysed HBV/HCV related tumors mostly resembled HBV-HCC. Indeed, lipid composition of non-tumorous HCV tissue, HCV tumors, HBV tumors and HBV/HCV tumors was highly similar. The tumor suppressor protein p53 regulates lipid metabolism. The p53 and p53S392 protein levels were induced in the tumors of HBV, HCV and double infected patients, and this was significant in HBV infection. Negative correlation of tumor p53 protein with free cholesterol indicates a role of p53 in cholesterol metabolism. In summary, the current study suggests that therapeutic strategies to target lipid metabolism in chronic viral hepatitis and associated cancers have to consider disease etiology.

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“…Although chemerin is protective in experimental models of HCC, chemerin was reported to be induced in tumor tissues of patients with HBV-related HCC [57].…”

Section: Chemerinmentioning

confidence: 99%

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

Chang

Yang

2020

IJMS

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Adipose tissue is a highly dynamic endocrine tissue and constitutes a central node in the interorgan crosstalk network through adipokines, which cause pleiotropic effects, including the modulation of angiogenesis, metabolism, and inflammation. Specifically, digestive cancers grow anatomically near adipose tissue. During their interaction with cancer cells, adipocytes are reprogrammed into cancer-associated adipocytes and secrete adipokines to affect tumor cells. Moreover, the liver is the central metabolic hub. Adipose tissue and the liver cooperatively regulate whole-body energy homeostasis via adipokines. Obesity, the excessive accumulation of adipose tissue due to hyperplasia and hypertrophy, is currently considered a global epidemic and is related to low-grade systemic inflammation characterized by altered adipokine regulation. Obesity-related digestive diseases, including gastroesophageal reflux disease, Barrett’s esophagus, esophageal cancer, colon polyps and cancer, non-alcoholic fatty liver disease, viral hepatitis-related diseases, cholelithiasis, gallbladder cancer, cholangiocarcinoma, pancreatic cancer, and diabetes, might cause specific alterations in adipokine profiles. These patterns and associated bases potentially contribute to the identification of prognostic biomarkers and therapeutic approaches for the associated digestive diseases. This review highlights important findings about altered adipokine profiles relevant to digestive diseases, including hepatic, pancreatic, gastrointestinal, and biliary tract diseases, with a perspective on clinical implications and mechanistic explorations.

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Chemerin Is Induced in Non-Alcoholic Fatty Liver Disease and Hepatitis B-Related Hepatocellular Carcinoma

Cited by 16 publications

References 42 publications

Identification of key genes and pathways in mild and severe nonalcoholic fatty liver disease by integrative analysis

Identification of key genes and pathways in mild and severe nonalcoholic fatty liver disease by integrative analysis

Liver Lipids of Patients with Hepatitis B and C and Associated Hepatocellular Carcinoma

Roles of Adipokines in Digestive Diseases: Markers of Inflammation, Metabolic Alteration and Disease Progression

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