LncRNA H19/microRNA-675/PPARα axis regulates liver cell injury and energy metabolism remodelling induced by hepatitis B X protein via Akt/mTOR signalling

Liu, Yiqing; Xu, Li; Lu, Bingru; Zhao, Mingqiu; Li, Li; Sun, Wei; Qiu, Zhanjun; Zhang, Bingchang

doi:10.1016/j.molimm.2019.09.006

Cited by 29 publications

(20 citation statements)

References 40 publications

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“… 55 Liu et al found that the lncRNA H19/miR‐675/PPARα axis might regulate liver cell injury and energy metabolism remodelling induced by HBx via Akt/mTOR signalling. 56 However, integrated and comprehensive analyses of the ceRNAs network in HBV infection have not sufficiently addressed these possibilities. In this study, we proposed a novel mRNA‐miRNA‐lncRNA triple‐regulatory network to explore potential ceRNA network interactions that may influence the process of CHB treatment.…”

Section: Discussionmentioning

confidence: 99%

Identifying potential biomarkers in hepatitis B virus infection and its response to the antiviral therapy by integrated bioinformatic analysis

Zhou

Wang

et al. 2021

J Cellular Molecular Medi

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Section: Discussionmentioning

confidence: 99%

Identifying potential biomarkers in hepatitis B virus infection and its response to the antiviral therapy by integrated bioinformatic analysis

Zhou

Wang

et al. 2021

J Cellular Molecular Medi

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“…As described earlier [Figure 1], HOTAIR is involved in PLK1-dependent proteasomal degradation of SUZ12 [53] , acting as scaffold in the antagonistic action of E3 ligase Mex3b vs. the PRC2 stabilizing function of RNA helicase DDX5 [64] . Other lncRNAs reported to be involved in HBVrelated liver cancer include lncRNA MALAT1 [94] and lncRNA H19 [95,96] , acting by regulating a set of miRNAs that activate AKT signaling, a mechanism relevant to HBV-related G2 liver tumors [54] . Recent studies have reported additional non-coding RNAs having a role in HBV-related HCC, acting via various mechanisms to affect hepatocarcinogenesis [76,97] , for example, the small nucleolar RNA SNOR18L5, mediating increased proteolysis of p53 [98] .…”

Section: Noncoding Rnas In Hbv-related Hccmentioning

confidence: 99%

Epigenetic mechanisms in hepatitis B virus-associated hepatocellular carcinoma

Andrisani¹

2021

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Chronic infection of the liver by the hepatitis B virus (HBV) is associated with increased risk for developing hepatocellular carcinoma (HCC). A multitude of studies have investigated the mechanism of liver cancer pathogenesis due to chronic HBV infection. Chronic inflammation, expression of specific viral proteins such as HBx, the integration site of the viral genome into the host genome, and the viral genotype, are key players contributing to HCC pathogenesis. In addition, the genetic background of the host and exposure to environmental carcinogens are also predisposing parameters in hepatocarcinogenesis. Despite the plethora of studies, the molecular mechanism of HCC pathogenesis remains incompletely understood. In this review, the focus is on epigenetic mechanisms involved in the pathogenesis of HBV-associated HCC. Epigenetic mechanisms are dynamic molecular processes that regulate gene expression without altering the host DNA, acting by modifying the host chromatin structure via covalent post-translational histone modifications, changing the DNA methylation status, expression of non-coding RNAs such as microRNAs and long noncoding RNAs, and altering the spatial, 3-D organization of the chromatin of the virus-infected cell. Herein, studies are described that provide evidence in support of deregulation of epigenetic mechanisms in the HBV-infected/-replicating hepatocyte and their contribution to hepatocyte transformation. In contrast to genetic mutations which are permanent, epigenetic alterations are dynamic and reversible. Accordingly, the identification of essential molecular epigenetic targets involved in HBV-mediated HCC pathogenesis offers the opportunity for the design and development of novel epigenetic therapeutic approaches.

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“…Long non-coding RNAs (lncRNAs), working as pivotal intracellular regulatory molecules, have functional bioactivity in various physiological processes (5). Crucially, lncRNAs have been proven to be pivotal regulators in tumor progression.…”

Section: Introductionmentioning

confidence: 99%

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

Qian

Garg

et al. 2020

Int J Oncol

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Colorectal cancer (CRC) is a tumor type characterized by high patient morbidity and mortality. It has been reported that long non-coding (lncRNA) LUNAR1 (LUNAR1) participates in the regulation of tumor progression, such as diffuse large B-cell lymphoma. However, its role and underlying mechanisms in CRC progression have not been elucidated. The present study was designed to investigate the underlying mechanisms by which LUNAR1 regulates CRC progression. RT-qPCR and Pearson's correlation analysis revealed that LUNAR1 was highly expressed and was negatively associated with the overall survival of CRC patients. Moreover, CCK-8, clone formation, wound-healing migration, Transwell chamber and FACs assay analyses showed that LUNAR1 knockdown inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. Additionally, LUNAR1 was found to function as a sponge of miR-495-3p, which was predicted by TargetScan and confirmed by luciferase reporter assay. Furthermore, functional studies indicated that miR-495-3p overexpression inhibited CRC cell proliferation, migration and invasion, while accelerating cell apoptosis. In addition, bioinformatics and luciferase reporter assays showed that miR-495-3p was found to negatively target Myc binding protein (MYCBP), and functional research showed that LUNAR1 accelerated CRC progression via the miR-495-3p/MYCBP axis. In conclusion, LUNAR1 accelerates CRC progression via the miR-495-3p/MYCBP axis, indicating that LUNAR1 may serve as a prognostic biomarker for CRC patients.

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LncRNA H19/microRNA-675/PPARα axis regulates liver cell injury and energy metabolism remodelling induced by hepatitis B X protein via Akt/mTOR signalling

Cited by 29 publications

References 40 publications

Identifying potential biomarkers in hepatitis B virus infection and its response to the antiviral therapy by integrated bioinformatic analysis

Identifying potential biomarkers in hepatitis B virus infection and its response to the antiviral therapy by integrated bioinformatic analysis

Epigenetic mechanisms in hepatitis B virus-associated hepatocellular carcinoma

lncRNA LUNAR1 accelerates colorectal cancer progression by targeting the miR‑495‑3p/MYCBP axis

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