Emerging role of miR-21 in non-alcoholic fatty liver disease

Benhamouche-Trouillet, Samira; Postic, Catherine

doi:10.1136/gutjnl-2015-310044

Cited by 26 publications

(19 citation statements)

References 10 publications

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“…In recent years, a large number of studies of NAFLD have been reported, which found that the mechanism of NAFLD has an association with the activation of proteinase 3, [ 21 ] miR-21, [ 22 ] and hepatokines. [ 23 ] NAFPD has some similar mechanisms to NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Transabdominal ultrasonography of the pancreas is superior to that of the liver for detection of ectopic fat deposits resulting from metabolic syndrome

Su²,

Lv³

et al. 2017

Medicine

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The aim of our study was to investigate the rate of nonalcoholic fatty pancreas disease (NAFPD) in the south China province of Fujian and its relationship to nonalcoholic fatty liver disease (NAFLD) and metabolic parameters.NAFPD is frequently identified on transabdominal ultrasound examination. The incidence of NAFPD varies from 16% to 69.7% depending on the country.A total of 256 subjects were recruited. Each was assessed by abdominal sonography to diagnose NAFLD and NAFPD. The ages, sexes, heights, weights, blood pressure, and detection of peripheral blood biochemical indices (cholesterol, triglycerides, high-density lipoprotein cholesterol [HDL], low-density lipoprotein cholesterol [LDL], and glucose) were recorded. The relationships among metabolic parameters and NAFPD or NAFLD were evaluated, and the positive rates of NAFLD and NAFPD in the general population were compared.The age, systolic blood pressure (SBP), diastolic blood pressure (DBP), body mass index (BMI), cholesterol, triglycerides, HDL, LDL, and glucose were significantly associated with NAFPD and NAFLD but the positive rate of NAFPD was significantly higher than that of NAFLD. The BMI, age, and NAFLD were the independent risk factors of NAFPD. The sex distribution, weight, SBP, DBP, BMI, LDL, HDL, triglycerides, glucose, cholesterol, NAFPD, and NAFLD were different significantly between metabolic syndrome and normal subjects.NAFPD and NAFLD can reflect the body metabolism, but NAFPD has a higher detection rate.

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Section: Discussionmentioning

confidence: 99%

Transabdominal ultrasonography of the pancreas is superior to that of the liver for detection of ectopic fat deposits resulting from metabolic syndrome

Su²,

Lv³

et al. 2017

Medicine

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“…Previous reports had shown that many miRNAs are closely related to NAFLD, including miR-122, miR-34a, miR-21 and so on [19][20][21]. In patients with NAFLD, miR-122 was associated with the fibrosis degree, and intrahepatic miR-122 in NAFLD patients was decreased but increased expression of miR-122 was observed in serum [19,22].…”

Section: Introductionmentioning

confidence: 88%

MiR-30b-5p regulates the lipid metabolism by targeting PPARGC1A in Huh-7 cell line

Zhang

Dong

et al. 2020

Lipids Health Dis

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Background: MiRNAs are a group of multifunctional non-coding RNAs which play an important role in the various physiological processes including the development of NAFLD. Recent studies have shown that miR-30b-5p tightly associated with the abnormal lipid metabolism in patients with NAFLD, but the detailed mechanism of miR-30b-5p in the lipid metabolism was remain unclear. The aim of this study was to investigate the effect of miR-30b-5p on the lipid metabolism in hepatocellular carcinoma Huh-7 cells. Material and methods: The correlation of intracellular fat content with the expression of miR-30b-5p in Huh-7 cells and HepG2 cells was investigated by treated cells with different concentrations of FFAs. The effect of miR-30b-5p on the lipid deposition in Huh-7 cells was tested by oil red O staining and TG concentrations measurement. qRT-PCR and western blot were used to investigate the lipid metabolism-related genes PPAR-α, SREBP-1, and GULT1 in miR-30b-5p overexpressed or inhibited Huh-7 cells. Target genes of miR-30b-5p were predicted using starBase, miRDB, and TargetScan databases and verified by qRT-PCR and western blot. Results: The expression of miR-30b-5p was significant decreased in the FFAs treated Huh-7 cells and HepG2 cells. Overexpressing miR-30b-5p in Huh-7 cells decreased the number and size of lipid droplets and intracellular TG concentrations in Huh-7 cells. Expression of fatty acid oxidation related gene PPAR-α was increased and expression of lipid synthesis related gene SREBP-1 was decreased in the miR-30b-5p overexpressed Huh-7 cells. In addition, miR-30b-5p regulates the intracellular lipid metabolism by targeting PPARGC1A. Conclusions: Overexpression of miR-30b-5p could reduce the intracellular fat deposition in Huh-7 cells, and miR-30b-5p might regulate the intracellular lipid metabolism by targeting the PPARGC1A in Huh-7 cells.

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“…These data indicated that HNK may reduce cell viability and induce apoptosis via inhibiting miR-21 expression in human OS cells. Previous studies also reported that HNK induces apoptosis and G 1 cell cycle arrest in various types of cancer cell ( 39 – 42 ). Furthermore, miR-21 has been identified as an important regulator of diverse cellular functions via the regulation of cancer cell growth ( 43 – 45 ).…”

Section: Discussionmentioning

confidence: 74%

Honokiol suppresses proliferation and induces apoptosis via regulation of the miR‑21/PTEN/PI3K/AKT signaling pathway in human osteosarcoma cells

2018

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Honokiol (HNK) is a small biphenolic compound, which exerts antineoplastic effects in various types of cancer. However, the mechanism underlying the antitumor effects of HNK in osteosarcoma (OS) cells is not yet fully understood. Emerging evidence has indicated that microRNAs (miRNAs/miRs) serve key roles in numerous pathological processes, including cancer. It has previously been reported that Chinese medicinal herbs harbor anticancer properties via modulating miRNA expression. Therefore, the present study aimed to determine whether HNK could suppress OS cell growth by regulating miRNA expression. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometric analysis were used to evaluate the cell proliferation and apoptosis in human OS cells after treatment with HNK, respectively. The results demonstrated that HNK inhibits proliferation and induces apoptosis of human OS cells in a dose-dependent manner. Furthermore, HNK-induced apoptosis was characterized by upregulation of proapoptotic proteins, including cleaved-caspase-3, cleaved-poly (ADP-ribose) polymerase and B-cell lymphoma 2 (Bcl-2)-associated X protein, and downregulation of the anti-apoptotic protein Bcl-2. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) verified that HNK was able to induce aberrant expression of miRNAs in human OS cells, and miR-21 was one of the miRNAs that was most significantly downregulated. To further investigate miR-21 function, the present study validated that HNK reduces miR-21 levels in a dose-dependent manner. In addition, restoration of miR-21 expression abrogated the suppressive effects of HNK on OS cells. Luciferase assay and western blot analysis identified that miR-21 inhibits the expression of phosphatase and tensin homolog (PTEN) by directly targeting its 3′-UTR. Notably, HNK was able to suppress the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway; however, it was reactivated by miR-21 overexpression. Taken together, these data indicated that HNK may inhibit proliferation and induce apoptosis of human OS cells by modulating the miR-21/PTEN/PI3K/AKT signaling pathway. Therefore, miR-21 may be considered a potential therapeutic target for the treatment of osteosarcoma with HNK.

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Emerging role of miR-21 in non-alcoholic fatty liver disease

Cited by 26 publications

References 10 publications

Transabdominal ultrasonography of the pancreas is superior to that of the liver for detection of ectopic fat deposits resulting from metabolic syndrome

Transabdominal ultrasonography of the pancreas is superior to that of the liver for detection of ectopic fat deposits resulting from metabolic syndrome

MiR-30b-5p regulates the lipid metabolism by targeting PPARGC1A in Huh-7 cell line

Honokiol suppresses proliferation and induces apoptosis via regulation of the miR‑21/PTEN/PI3K/AKT signaling pathway in human osteosarcoma cells

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