Identification of Characteristic Genomic Markers in Human Hepatoma HuH-7 and Huh7.5.1-8 Cell Lines

Kawamoto, Masaki; Yamaji, Taiki; Saito, Kyoko; Shirasago, Yoshitaka; Satomura, Kazuhiro; Endo, Toshinori; Fukasawa, Masayoshi; Hanada, Kentaro; Osada, Naoki

doi:10.3389/fgene.2020.546106

Cited by 33 publications

(23 citation statements)

References 51 publications

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“…Notably, hepatitis C virus (HCV) infection is one of the leading etiological agents resulting in progressive liver fibrosis [ 32 , 33 ]. Therefore, we analyzed the expression of HSD17B13 after HCV infection in Huh7.5 cells, a hepatocyte cell line that strongly supports HCV infection and replication [ 34 , 35 ]. After three days of HCV infection, HSD17B13 expression was increased and paralleled with HCV viral loads ( Figure 2 E,F).…”

Section: Resultsmentioning

confidence: 99%

Down-Regulating the High Level of 17-Beta-Hydroxysteroid Dehydrogenase 13 Plays a Therapeutic Role for Non-Alcoholic Fatty Liver Disease

Wang

et al. 2022

IJMS

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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and there is no specific drug to treat it. Recent results showed that 17-beta-hydroxysteroid dehydrogenase type 13 (HSD17B13) is associated with liver diseases, but these conclusions are controversial. Here, we showed that HSD17B13 was more highly expressed in the livers of NAFLD patients, and high expression was induced in the livers of murine NAFLD models and cultural hepatocytes treated using various etiologies. The high HSD17B13 expression in the hepatocytes facilitated the progression of NAFLD by directly stabilizing the intracellular lipid drops and by indirectly activating hepatic stellate cells. When HSD17B13 was overexpressed in the liver, it aggravated liver steatosis and fibrosis in mice fed with a high-fat diet, while down-regulated the high expression of HSD17B13 by short hairpin RNAs produced a therapeutic effect in the NAFLD mice. We concluded that high HSD17B13 expression is a good target for the development of drugs to treat NAFLD.

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Section: Resultsmentioning

confidence: 99%

Down-Regulating the High Level of 17-Beta-Hydroxysteroid Dehydrogenase 13 Plays a Therapeutic Role for Non-Alcoholic Fatty Liver Disease

Wang

et al. 2022

IJMS

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“…JFH1 T is unlike other HCV patient isolates in that it replicates in cell culture without adaptive mutations or modifications of the cells ( 69 ). Huh-7.5 cells are cancer-derived and are widely known to have deficiencies in pathways involved in innate immunity ( 70 , 71 ). Due to these limitations, any findings presented here should be verified by using in vivo animal studies and biopsies from HCV-infected patients.…”

Section: Discussionmentioning

confidence: 99%

Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death

et al. 2022

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Extensive inflammation in the liver is known to contribute to the pathogenesis of hepatitis C virus (HCV) infection. Apoptosis has, for a long time, been known to act as a mechanism of hepatocyte death, but our previous research also identified inflammasome-mediated pyroptosis in infected and uninfected bystander cells as an additional mechanism of HCV-induced cytopathicity. The purpose of this study was to investigate the mechanism of HCV-induced cell death and to determine the timing and relative contributions of apoptosis and pyroptosis during HCV infection. In a model employing a cell culture-adapted strain of JFH-1 HCV and Huh-7.5 hepatocyte-like cells, we found that pyroptosis occurred earlier than did apoptosis during infection. CRISPR knockout of NLRP3 resulted in decreased caspase-1 activation, but not complete elimination, indicating multiple sensors are likely involved in HCV-induced pyroptosis. Knockout of gasdermin-D resulted in increased activation of apoptosis-related caspase-3, suggesting potential crosstalk between the two cell death pathways. An unexpected decrease in activated caspase-1 levels was observed when caspase-3 was knocked out, implying that caspase-3 may have a role in the initiation of pyroptosis, at least in the context of HCV infection. Lower viral titres in culture fluids and increased ratios of intracellular to extracellular levels of infectious virus were observed in knockout versus wild-type Huh-7.5 cells, suggesting that HCV may induce programmed cell death in order to enhance virus release from infected cells. These results contribute to the understanding of HCV pathogenesis and add to the increasing volume of literature suggesting various programmed cell death pathways are not mutually exclusive.

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“…FAK ( 32 , 38 , 39 ), ROCK2 ( 32 , 40 ), and CCND1 ( 32 , 41 ) have all been previously shown to be direct targets of miR-138; therefore, it is not surprising that we found their expression changed in the fibroblasts that had an altered miR-138 expression. Taken together, our findings suggest that they act in cohort to control fibroblast migration, and that their expression is regulated by miR-138.…”

Section: Discussionmentioning

confidence: 58%

MicroRNA-138 Abates Fibroblast Motility With Effect on Invasion of Adjacent Cancer Cells

et al. 2022

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BackgroundRecent studies have shown aberrant expression of micro-RNAs in cancer-associated fibroblasts (CAFs). This study aimed to investigate miR-138 dysregulation in CAFs in oral squamous cell carcinoma (OSCC) and its effects on their phenotype and invasion of adjacent OSCC cells.MethodsExpression of miR-138 was first investigated in OSCC lesions (n = 53) and OSCC-derived CAFs (n = 15). MiR-138 mimics and inhibitors were used to functionally investigate the role of miR-138 on CAF phenotype and the resulting change in their ability to support OSCC invasion.ResultsExpression of miR-138 showed marked heterogeneity in both OSCC tissues and cultured fibroblasts. Ectopic miR-138 expression reduced fibroblasts’ motility and collagen contraction ability and suppressed invasion of suprajacent OSCC cells, while its inhibition resulted in the opposite outcome. Transcript and protein examination after modulation of miR-138 expression showed changes in CAF phenotype-specific molecules, focal adhesion kinase axis, and TGFβ1 signaling pathway.ConclusionsDespite its heterogeneous expression, miR-138 in OSCC-derived CAFs exhibits a tumor-suppressive function.

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Identification of Characteristic Genomic Markers in Human Hepatoma HuH-7 and Huh7.5.1-8 Cell Lines

Cited by 33 publications

References 51 publications

Down-Regulating the High Level of 17-Beta-Hydroxysteroid Dehydrogenase 13 Plays a Therapeutic Role for Non-Alcoholic Fatty Liver Disease

Down-Regulating the High Level of 17-Beta-Hydroxysteroid Dehydrogenase 13 Plays a Therapeutic Role for Non-Alcoholic Fatty Liver Disease

Crosstalk Between Pyroptosis and Apoptosis in Hepatitis C Virus-induced Cell Death

MicroRNA-138 Abates Fibroblast Motility With Effect on Invasion of Adjacent Cancer Cells

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