MicroRNAs in hepatic pathophysiology

Murakami, Yoshiki; Kawada, Norifumi

doi:10.1111/hepr.12730

Cited by 56 publications

(50 citation statements)

References 87 publications

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“…They can play an important role in the pathogenesis and prognosis of chronic infection. Several studies have shown interactions between HCV and host miRNAs . miRNA‐21 is an “onco‐miRNA,” and it is frequently overexpressed in solid tumors and is upregulated in liver fibrosis .…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have shown interactions between HCV and host miRNAs . miRNA‐21 is an “onco‐miRNA,” and it is frequently overexpressed in solid tumors and is upregulated in liver fibrosis . Additionally, there is a relationship between TGF‐β, critical factor in the development of liver fibrosis, signaling and miRNA‐21, where TGF‐β stimulates the processing of miRNA‐21 precursor into mature miRNA‐21 and miRNA‐21 represses SMAD7, the negative regulator of TGF‐β signaling, promoting effects of TGF‐β …”

Section: Discussionmentioning

confidence: 99%

“…miRNA‐21 is one of the earliest identified cancer‐promoting miRNAs (oncomiRs). It is upregulated in liver fibrosis . This is assumed to be based on the pro‐fibrogenic stimulation of TGF‐β to Smad‐3 which is crucial for miRNA‐21 transcription .…”

Section: Introductionmentioning

confidence: 99%

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Relation between microRNA‐21, transforming growth factor β and response to treatment among chronic hepatitis C patients

Ghazy

Osman

Rashwan

et al. 2019

Journal of Medical Virology

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Background Persistence of hepatitis C virus (HCV) infection and response to antiviral therapy has been shown to be associated with inappropriate levels of cytokines and microRNAs (miRNAs). miRNA levels have been reported to fluctuate during treatment. Thus they could be useful predictors for responses to treatment among HCV infected patients, thereby reducing ineffective treatments. Aim The current study aimed to investigate the relation between miRNA‐21 expression profiles, transforming growth factor β (TGF‐β) serum levels and response to treatment with the new direct antiviral drugs (sofosbuvir + daclatasvir ± ribavirin), among HCV infected Egyptian patients. Subjects and Methods This prospective study was conducted on 50 HCV infected patients (before and after treatment) and 20 healthy volunteers. miRNA expression profiles were determined by real‐time polymerase chain reaction and TGF‐β1 serum levels were measured by using enzyme‐linked immunosorbent assay. Results There was a significant increase in serum albumin, platelets count and a significant decrease in liver enzymes, serum bilirubin, and prothrombin time after treatment. Significant reduction of viral load among HCV patients after receiving the treatment was reported. Concomitantly, there was an increase in the relative quantity of miRNA‐21 (P = .001*) and serum levels of TGF‐β1 ( P = .337) among HCV patients after receiving treatment. Conclusion Nearly all responders to direct antiviral drugs showed increased levels of both miRNA‐21 and TGF‐β1. This may indicate an interplay between TGF‐β1 and miRNA‐21 during remission or progression of viral infection. Thus miRNA‐21 could be used as promising serum biomarker, for assessment of antiviral treatment efficacy and improvement of fibrosis among chronically infected HCV patients.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Relation between microRNA‐21, transforming growth factor β and response to treatment among chronic hepatitis C patients

Ghazy

Osman

Rashwan

et al. 2019

Journal of Medical Virology

View full text Add to dashboard Cite

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“…Several studies have reported that the post‐transcriptional regulation of lncRNAs could modulate gene transcription by interaction with RNA‐binding proteins, or function as competing endogenous RNAs (ceRNA) by competitively binding common miRNAs to influence the accumulation of miRNA and, in turn, affect its targets . The aberrant expression of miRNAs in hepatic tissue was related to the pathogenesis of liver disease, including viral hepatitis, HCC, and fatty liver disease . Therefore, Starbase (http://starbase.sysu.edu.cn/index.php) was used to predict and select the miRNAs that interacted with miR143HG.…”

Section: Resultsmentioning

confidence: 91%

Long non‐coding RNA miR143HG predicts good prognosis and inhibits tumor multiplication and metastasis by suppressing mitogen‐activated protein kinase and Wnt signaling pathways in hepatocellular carcinoma

Xiong

Chen

et al. 2019

Hepatology Research

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Aim The expression of microRNA143HG (miR143HG) was significantly downregulated in hepatocellular carcinoma (HCC) tissues by bioinformatics analysis. This study aimed to determine the role of miR143HG in HCC cell proliferation and metastasis. Methods Fifty patients with HCC were divided into two groups based on median miR143HG expression levels. The correlation between miR143HG expression and prognosis, and the correlations between miR143HG expression and the patients’ clinicopathological characteristics were evaluated based on the two groups. Gain‐of‐function and loss‐of‐function measurements of miR143HG were carried out to verify the biological function of miR143HG by Cell Counting Kit‐8, EdU, Transwell, and western blotting assays and flow cytometric analysis. The underlying mechanism was explored by quantitative real‐time polymerase chain reaction of miRNA (miR‐155‐5p and miR‐26b‐5p), luciferase reporter assay, western blotting of Wnt signaling pathway‐related proteins (β‐catenin, adenomatous polyposis coli (APC), glycogen synthase kinase 3β (GSK3β), ZEB1, and E‐cadherin), mitogen‐activated protein kinase (MAPK) signaling pathway‐related proteins (extracellular signal‐regulated kinase [ERK]1/2, p‐ERK1/2, c‐Jun N‐terminal kinase (JNK), p‐JNK, P38, and p‐P38), and immunofluorescence staining of β‐catenin. Results miR143HG expression was markedly downregulated in HCC tissues and cells. Its expression was associated with the presence or absence of portal vein tumor thrombus, hepatitis B virus infection, relapse and metastasis, and Barcelona Clinic Liver Cancer stage. Additionally, miR143HG expression predicted a good prognosis and acted as an independent prognostic factor in HCC for overall survival. Overexpression of miR143HG suppressed HCC cell proliferation and metastasis, and induced cell cycle arrest and apoptosis. Consistently, the depletion of miR143HG resulted in the opposite phenomenon of the aforementioned results. miR143HG inhibits miR‐155 expression; miR‐155 directly targets APC, which is a negative regulator of the Wnt/β‐catenin pathway, so miR143HG can act on the Wnt pathway. miR143HG was further found to reduce the expression of β‐catenin and block the nuclear accumulation of β‐catenin, ultimately inhibiting the activation of the Wnt pathway. It inhibits the expression of Wnt downstream target gene ZEB1, and then E‐cadherin expression is increased and cell motility is inhibited. Furthermore, miR143HG exerts its antiproliferative function by influencing the MAPK signaling pathway and then inducing G2/M arrest in cells. Conclusion This study showed that miR143HG plays critical roles in the development and progression of HCC by suppressing the MAPK and Wnt signaling pathways.

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“…Aberrant expression of miRNAs in liver tissue was described for the pathogenesis of several liver diseases, including viral hepatitis, nonalcoholic fatty liver disease, alcohol-induced liver damage and, particularly, hepatocellular carcinoma. 4 Published data on alcoholic hepatitis (AH) have been limited to experimental studies in rodents so far. 5 6 In this issue of Gut, Blaya et al 7 add important information to the existing knowledge via a carefully executed systematic profiling analysis of miRNAs in human alcoholic hepatitis (AH) and their experimental translation in several animal models involving toxic and alcohol-mediated liver injury, and cell culture.…”

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confidence: 99%