The miR-139-5p/peripheral myelin protein 22 axis modulates TGF-β-induced hepatic stellate cell activation and CCl4-induced hepatic fibrosis in mice

He, Chao; Shu, Bo; Zhou, Yingxia; Zhang, Ruizhi; Yang, Xin

doi:10.1016/j.lfs.2021.119294

Cited by 6 publications

(4 citation statements)

References 49 publications

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“…Although the genes in this family are commonly implicated in cancer cell migration, proliferation, and differentiation, few studies have demonstrated their role in fibrosis. He et al previously discovered that abnormal upregulation of PMP22 in TGF- β -activated HSCs and CCl 4 -induced hepatic fibrosis model in mice, as well as the pro-fibrotic role of PMP22 through aggravating TGF- β -induced HSC activation [ 31 ]. It would be interesting to look into and compare the role of the entire gene family in fibrotic processes in the liver.…”

Section: Discussionmentioning

confidence: 99%

EMP1 as a Potential Biomarker in Liver Fibrosis: A Bioinformatics Analysis

Chen

Han

et al. 2023

Gastroenterology Research and Practice

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Liver fibrosis is a wound-healing response to chronic injury, which may result in cirrhosis and liver failure. Studies have been carried on the mechanisms and pathogenesis of liver fibrosis. However, the potential cell-specific expressed marker genes involved in fibrotic processes remain unknown. In this study, we combined a publicly accessible single-cell transcriptome of human liver with microarray datasets to evaluate the cell-specific expression patterns of differentially expressed genes in the liver. We noticed that EMP1 (epithelial membrane protein 1) is significantly active not only in CCl4 (carbon tetrachloride)-treated mouse liver fibrosis but also in BDL (bile duct ligation)-induced liver fibrosis and even in human fibrotic liver tissues such as alcoholic hepatitis, NASH (nonalcoholic steatohepatitis), and advanced stage liver fibrosis. Furthermore, we demonstrated that EMP1 is a specific fibrotic gene expressed in HSCs (hepatic stellate cells) and endothelial cells using the Protein Atlas single-cell transcriptome RNA-sequencing clustering. Its expression was significantly elevated in fibrotic HSCs or CCl4 and NASH-induced fibroblasts. Previous research revealed that EMP1 plays a role in proliferation, migration, metastasis, and tumorigeneses in different cancers via a variety of mechanisms. Because HSC activation and proliferation are two important steps following liver injury, it would be interesting to investigate the role of EMP1 in these processes. All of this information suggested that EMP1 could be used as a novel fibrotic liver marker and a possible target in the future.

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Section: Discussionmentioning

confidence: 99%

EMP1 as a Potential Biomarker in Liver Fibrosis: A Bioinformatics Analysis

Chen

Han

et al. 2023

Gastroenterology Research and Practice

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“…Interestingly, the miRNAs that regulate HSCs phenotype were consistently reversed with a concomitant decrease in hepatic ECM deposition. miRNAs that activate HSCs (miR-199a-3p and miR-214-3p) were significantly suppressed (Ma et al, 2018;Yang et al, 2020), while those restrain the proliferation and activation of HSCs (miR-378a-3p, miR-139-5p, miR-455-3p, and miR-193a-3p) were remarkably increased during the fibrosis regression (Hyun et al, 2016;Ju et al, 2019;Wei et al, 2019;He et al, 2021). Among the differentially (mmu-miR-1843a-5p, mmu-miR-193a-5p, mmu-miR-194-2-3p, and mmu-miR-30c-2-3p) and their target genes.…”

Section: Discussionmentioning

confidence: 99%

Integrated Analysis of Hepatic miRNA and mRNA Expression Profiles in the Spontaneous Reversal Process of Liver Fibrosis

et al. 2021

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Liver fibrosis results from the imbalance between extracellular matrix (ECM) production and degradation, which is a common pathological consequence of various chronic liver diseases. Although many miRNAs have been reported in liver fibrosis progression, miRNA-mRNA interactions in its reversal process remain to be elucidated. In the current study, we performed an integrated analysis of miRNA and mRNA expression profiles in the mouse model with the spontaneous reversal potency of liver fibrosis. A total of 102 miRNA and 2,845 mRNAs showed significant differential expression in reversal mice compared to fibrotic mice. Moreover, 3,769 putative negatively correlated miRNA-mRNA pairs were revealed to be potentially implicated in the biological function regulation of small molecule metabolism and ECM organization. By integrating miRNA-mRNA regulatory networks, mmu-miR-1843a-5p, mmu-miR-193a-5p, mmu-miR-194-2-3p, and mmu-miR-30c-2-3p were identified as lysyl oxidases-specific miRNAs that were correlated with fibrosis reversal. Our results provided potential candidate targets for the treatment of liver fibrosis.

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“…Since the pathway to HCC most often stems from fibrosis, it has been found that the otherwise quiescent phenotype, HSCs, are constitutively activated, which transdifferentiate into myofibroblasts with enhanced ECM production. 111 Another component of HCC TME is extracellular vesicles (EVs) secreted by cancer cells and stromal cells. They are essential for HCC malignancy and serve as biomarkers for early diagnosis.…”

Section: Tme Alteration In Hcc Contributes To Deranged Metabolismmentioning

confidence: 99%

Unraveling the Sweet Secrets of HCC: Glucometabolic Rewiring in Hepatocellular Carcinoma

Bhat,

Farooq,

Ismail

et al. 2023

Technol Cancer Res Treat

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Hepatocellular carcinoma (HCC) is the primary form of liver cancer. It causes ∼ 800 000 deaths per year, which is expected to increase due to increasing rates of obesity and metabolic dysfunction associated steatotic liver disease (MASLD). Current therapies include immune checkpoint inhibitors, tyrosine kinase inhibitors, and monoclonal antibodies, but these therapies are not satisfactorily effective and often come with multiple side effects and recurrences. Metabolic reprogramming plays a significant role in HCC progression and is often conserved between tumor types. Thus, targeting rewired metabolic pathways could provide an attractive option for targeting tumor cells alone or in conjunction with existing treatments. Therefore, there is an urgent need to identify novel targets involved in cancer-mediated metabolic reprogramming in HCC. In this review, we provide an overview of molecular rewiring and metabolic reprogramming of glucose metabolism in HCC to understand better the concepts that might widen the therapeutic window against this deadly cancer.

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The miR-139-5p/peripheral myelin protein 22 axis modulates TGF-β-induced hepatic stellate cell activation and CCl4-induced hepatic fibrosis in mice

Cited by 6 publications

References 49 publications

EMP1 as a Potential Biomarker in Liver Fibrosis: A Bioinformatics Analysis

EMP1 as a Potential Biomarker in Liver Fibrosis: A Bioinformatics Analysis

Integrated Analysis of Hepatic miRNA and mRNA Expression Profiles in the Spontaneous Reversal Process of Liver Fibrosis

Unraveling the Sweet Secrets of HCC: Glucometabolic Rewiring in Hepatocellular Carcinoma

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