Association between hepatitis B virus and MHC class I polypeptide-related chain A in human hepatocytes derived from human-mouse chimeric mouse liver

Sasaki, Reina; Wu, Shuang; Nakamoto, Shingo; Haga, Yuki; Jiang, Xia; Nakamura, Masato; Shirasawa, Hiroshi; Yokosuka, Osamu

doi:10.1016/j.bbrc.2015.07.102

Cited by 12 publications

(21 citation statements)

References 27 publications

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“…Huh7, HepG2 and HepG2.2.15 were previously reported [11, 12]. Huh6 and PLC/PRF/5 were purchased from the National Institutes of Biomedical Innovation, Health and Nutrition JCRB Cell Bank (Ibaraki, Osaka, Japan).…”

Section: Methodsmentioning

confidence: 99%

Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines

et al. 2017

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BackgroundDespite recent advances in treatment strategies, it is still difficult to cure patients with hepatocellular carcinoma (HCC). Sorafenib is the only approved multiple kinase inhibitor for systemic chemotherapy in patients with advanced HCC. The majority of advanced HCC patients are resistant to sorafenib. The mechanisms of sorafenib resistance are still unknown.MethodsThe expression of molecules involved in the mitogen-activated protein kinase (MAPK) signaling pathway in human hepatoma cell lines was examined in the presence or absence of sorafenib. Apoptosis of human hepatoma cells treated with sorafenib was investigated, and the expression of Jun proto-oncogene (c-Jun) was measured.ResultsThe expression and phosphorylation of c-Jun were enhanced in human hepatoma cell lines after treatment with sorafenib. Inhibiting c-Jun enhanced sorafenib-induced apoptosis. The overexpression of c-Jun impaired sorafenib-induced apoptosis. The expression of osteopontin, one of the established AP-1 target genes, was enhanced after treatment with sorafenib in human hepatoma cell lines.ConclusionsThe protein c-Jun plays a role in sorafenib resistance in human hepatoma cell lines. The modulation and phosphorylation of c-Jun could be a new therapeutic option for enhancing responsiveness to sorafenib. Modulating c-Jun may be useful for certain HCC patients with sorafenib resistance.

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Section: Methodsmentioning

confidence: 99%

Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines

et al. 2017

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“…Human hepatocyte PXB cells (PhoenixBio, Higashi-Hiroshima, Japan) [ 24 ] were derived from chimeric mice with hepatocyte-humanized livers (PXB-mouse). PXB cells were cultured without passage as described previously [ 24 ], and maintained in DMEM supplemented with 2% FBS, 20 mM HEPES, 44 mM NaHCO3, 15 μg/mL L-proline, 0.25 μg/mL insulin, 50 nM dexamethasone, 5 ng/mL EGF, 0.1 mM Asc-2P and 2% DMSO (2% DMSO-supplemented hepatocyte clonal growth medium (dHCGM)).…”

Section: Methodsmentioning

confidence: 99%

“…Conditioned media were clarified by centrifugation at 5,000 g to remove cell debris, and stored at -20°C until use. HBV genotype C isolates were purchased from PhoenixBio [ 24 ]. Informed consent from the patient was obtained by Prof. Yasuhito Tanaka, Nagoya City University, Japan [ 24 ].…”

Section: Methodsmentioning

confidence: 99%

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Possible Involvement of Hepatitis B Virus Infection of Hepatocytes in the Attenuation of Apoptosis in Hepatic Stellate Cells

et al. 2016

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BackgroundThe induction of apoptosis in hepatic stellate cells (HSCs) is a promising therapeutic strategy against hepatitis B virus (HBV)-related hepatic fibrosis. The underlying mechanisms of apoptosis in HSCs, however, are unknown under consideration of HBV infection. In this study, the effects of HBV on apoptosis and endoplasmic reticulum (ER) stress signaling in HSCs were examined.MethodsThe effects of conditioned media (CM) from HepG2.2.15 on apoptosis induced by the proteasome inhibitor MG132 in LX-2 and HHSteC were studied in regard to c-Jun. In combination with c-Fos, c-Jun forms the AP-1 early response transcription factor, leading to AP-1 activation, signal transduction, endoplasmic reticulum (ER) stress and apoptosis.ResultsIn LX-2 cells, MG132 treatment was associated with the phosphorylation of c-Jun, activation of AP-1 and apoptosis. However, in the presence of CM from HepG2.2.15, these phenomena were attenuated. In HHSteC cells, similar results were observed. HBV genomic DNA is not involved in the process of HSC apoptosis. It is possible that HBeAg has an inhibitory effect on MG132-induced apoptosis in LX-2. We also observed the upregulation of several ER stress-associated genes, such as cAMP responsive element binding protein 3-like 3, inhibin-beta A and solute carrier family 17-member 2, in the presence of CM from HepG2.2.15, or CM from PXB cells infected with HBV.ConclusionsHBV inhibits the activation of c-Jun/AP-1 in HSCs, contributing to the attenuation of apoptosis and resulting in hepatic fibrosis. HBV also up-regulated several ER stress genes associated with cell growth and fibrosis. These mechanistic insights might shed new light on a treatment strategy for HBV-associated hepatic fibrosis.

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“…Human hepatoma cell lines (HepG2 and Huh7), hepatic stellate cell line LX-2 and human pancreatic cancer MIAPaCa-2 cells were maintained in Roswell Park Memorial Institute medium (RPMI 1640) (Sigma, St. Louis, MO, USA) supplemented with 1-10% fetal bovine serum, penicillin (100 U/mL) and streptomycin (100 μg/mL) at 5% CO2 and 37°C. HepG2, Huh7 and MIAPaCa-2 cells were purchased from the Japanese Collection of Research Bioresources Cell Bank (Ibaraki, Osaka, Japan) [26,51]. LX-2 cells, spontaneously immortalized cells, were kindly provided by Prof. Scott L. Friedman, Mount Sinai Medical School, NY, USA [52].…”

Section: Cell Lines and Reagentsmentioning

confidence: 99%

Possible association of arrestin domain-containing protein 3 and progression of non-alcoholic fatty liver disease

Ogawa¹,

Higuchi²,

Takahashi³

et al. 2019

Int. J. Med. Sci.

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909 I In nt te er rn na at ti io on na al l J Jo ou ur rn na al l o of f M Me ed di ic ca al l S Sc ci ie en nc ce es s 2019; 16(7): 909-921. AbstractThe prevalence of non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH) is increasing worldwide. Several effective drugs for these diseases are now in development and under clinical trials. It is important to reveal the mechanism of the development of NAFLD and NASH. We investigated the role of arrestin domain-containing protein 3 (ARRDC3), which is linked to obesity in men and regulates body mass, adiposity and energy expenditure, in the progression of NAFLD and NASH. We performed knockdown of endogenous ARRDC3 in human hepatocytes and examined the inflammasome-associated gene expression by real-time PCR-based array. We also examined the effect of conditioned medium from endogenous ARRDC3-knockdown-hepatocytes on the apoptosis of hepatic stellate cells. We observed that free acids enhanced the expression of ARRDC3 in hepatocytes. Knockdown of ARRDC3 could lead to the inhibition of inflammasome-associated gene expression in hepatocytes. We also observed that conditioned medium from endogenous ARRDC3-knockdown-hepatocytes enhances the apoptosis of hepatic stellate cells. ARRDC3 has a role in the progression of NAFLD and NASH and is one of the targets for the development of the effective treatment of NAFLD and NASH.

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Association between hepatitis B virus and MHC class I polypeptide-related chain A in human hepatocytes derived from human-mouse chimeric mouse liver

Cited by 12 publications

References 27 publications

Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines

Overexpression of c-Jun contributes to sorafenib resistance in human hepatoma cell lines

Possible Involvement of Hepatitis B Virus Infection of Hepatocytes in the Attenuation of Apoptosis in Hepatic Stellate Cells

Possible association of arrestin domain-containing protein 3 and progression of non-alcoholic fatty liver disease

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