The transcription factor c-JUN/AP-1 promotes HBV-related liver tumorigenesis in mice

Trierweiler, Claudia; Hockenjos, Birgit; Zatloukal, Kurt; Thimme, Robert; Blum, Hubert E.; Wagner, Erwin F.; Hasselblatt, Peter

doi:10.1038/cdd.2015.121

Cited by 54 publications

(52 citation statements)

References 32 publications

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“…DNA methylation, histone modification, nucleosome remodeling, and RNA‐mediated targeting regulate many biological processes . These modifications are interpreted by proteins that recognize a particular modification and facilitate the appropriate downstream biological effects …”

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“…(10,11) These modifications are interpreted by proteins that recognize a particular modification and facilitate the appropriate downstream biological effects. (12)(13)(14) As a key viral oncoprotein, HBx plays crucial roles in the development of hepatocellular carcinoma (HCC), (15,16) whose primary role is to enhance the transformation of liver cell because of its activities on cell cycle regulation, signaling pathways and DNA repair. (17,18) It is rather remarkable that HBx is particularly required for HBV replication, which accomplishes this task by an unusual mechanism, enhancing transcription from extrachromosomal DNA templates through recruitment of HBx partners CBP, P300, and PCAF to cccDNA.…”

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confidence: 99%

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Hepatitis B virus X protein–elevated MSL2 modulates hepatitis B virus covalently closed circular DNA by inducing degradation of APOBEC3B to enhance hepatocarcinogenesis

et al. 2017

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Hepatitis B virus X protein–elevated MSL2 modulates hepatitis B virus covalently closed circular DNA by inducing degradation of APOBEC3B to enhance hepatocarcinogenesis

et al. 2017

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“…https://www.ebi.ac.uk/intact/interactors/id:Q92878*). C-Jun induces HBV-related liver tumourigenesis in mice via upregulating the transcription of its target geneosteopontin (OPN) [11]. OPN is overexpressed in several human carcinomas and contributes to inflammation, tumour progression, and metastasis [12].…”

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confidence: 99%

RAD50 predicts the prognosis of hepatitis B virus-related hepatocellular carcinoma

Liu

Chen

et al. 2020

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Background Increasing evidence indicates that RAD50, which is involved in the DNA double-strand break (DSB) repair process, is also involved in cancer outcomes. However, its role in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) remains unclear.Aim This study was designed to investigate the expression of RAD50 and its prognostic value in HCC patients.Method A total of 207 patientswith HBV-associated HCCfrom two cohorts (107 and 100 patientsfrom the Affiliated Hospital of Youjiang Medical University of Nationalities and the Affiliated Hospital of Nantong University, respectively) were enrolled in the current study.The distribution of the categorical clinical-pathological data and the levels of RAD50 expression were compared with a χ 2 test. IHC staining of RAD50 was performed.A partial likelihood test based onunivariate and multivariate Cox regression analysis was developed to address the influence of independent factors on disease-free survival (DFS) and overall survival (OS). The Oncomine online database was used to analyse and validate the differential expression of RAD50. The Kaplan-Meier method and a log-rank test were performed to assess the influence of RAD50 on survival at different levels.Results RAD50 was highly expressed in HCC tissues compared to normal tissues and was significantly correlated with OS in the TCGA cohort. The validation analysis indicated that significantly increased levels of RAD50 were expressed in HCC tissues in the two independent cohorts, AHYMUN and AHNTU. In addition, HCC patients with elevated RAD50 expression levels showed poor OS and DFSin the AHYMUN cohort and decreased OS and DF Sin the AHNTU cohort. Furthermore, four datasets obtained from the Oncomine database validated the analysis of the differential expression of RAD50 in HCC tumours and normal tissues.Discussion In our study, we demonstrated that RAD50 was positively correlated with poor prognosis in HCC patients in the TCGA cohort. Our study also suggested that increased RAD50 expression in HBV-related HCC is a marker of poor prognosis. In this study, the analysis of the data form the two cohorts supported our hypothesis and clearly demonstrated thehigh expression of RAD50 in tumour tissues from HCC patients, which results inincreases in the HCC recurrence rate and poor overall survival.

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“…According to the IntAct molecular interaction database, human RAD50 potentially interacts with the transcription factor c-Jun/activator protein 1 (AP-1) (website: https://www.ebi.ac.uk/intact/interactors/id:Q92878*). C-Jun induces HBV-related liver tumourigenesis in mice via upregulating the transcription of its target gene osteopontin (OPN) (15). OPN is overexpressed in several human carcinomas and contributes to inflammation, tumour progression, and metastasis (16,17).…”

Section: Discussionmentioning

confidence: 99%

RAD50 predicts the prognosis of hepatitis B virus-related hepatocellular carcinoma

Liu

Chen

et al. 2019

Preprint

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RAD50, which is involved in the DNA double-strand break (DSB) repair process, is also involved in cancer outcomes. However, its role in hepatitis B virus (HBV)-associated hepatocellular carcinoma (HCC) remains unclear. RAD50 increased in HCC tissues compared to normal tissues and was correlated with OS in the TCGA cohort. The validation analysis indicated that increased RAD50 was expressed in HCC tissues in the two independent cohorts, 107 and 100 patients from the Affiliated Hospital of Youjiang Medical University of Nationalities (AHYMUN) and the Affiliated Hospital of Nantong University (AHNTU), respectively. In addition, HCC patients with elevated RAD50 expression showed poor OS and DFS in the AHYMUN cohort and decreased OS and DFS in the AHNTU cohort. Furthermore, four datasets obtained from the Oncomine database validated the analysis of the differential expression of RAD50 in HCC tumors and normal tissues. In conclusion, our study reveals that elevated RAD50 expression is correlated with cancer progression and poor survival in HBV-related HCC patients. These data suggest that RAD50 may act as an oncogene and may serve as a promising therapeutic target for HCC patients.

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The transcription factor c-JUN/AP-1 promotes HBV-related liver tumorigenesis in mice

Cited by 54 publications

References 32 publications

Hepatitis B virus X protein–elevated MSL2 modulates hepatitis B virus covalently closed circular DNA by inducing degradation of APOBEC3B to enhance hepatocarcinogenesis

Hepatitis B virus X protein–elevated MSL2 modulates hepatitis B virus covalently closed circular DNA by inducing degradation of APOBEC3B to enhance hepatocarcinogenesis

RAD50 predicts the prognosis of hepatitis B virus-related hepatocellular carcinoma

RAD50 predicts the prognosis of hepatitis B virus-related hepatocellular carcinoma

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