The search for the hepatitis B virus genome in cells of human hepatocellular carcinoma cell lines.

Fujise, Kiyotaka; Fujita, Kazunobu; Nagamori, Seishi; Hasumura, Satoshi; Homma, Sadamu; Sujino, H; Matsuura, Tomokazu; Shimizu, Keiichirou; Niiya, Minoru; Ohno, Tsuneya; Kameda, Haruo

doi:10.2957/kanzo.29.697

Cited by 38 publications

(55 citation statements)

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“…Hepatocellular carcinoma cell line, JHH7 cells were kindly supplied by Dr. Matsuura (Jikei University School of Medicine, Tokyo, Japan) in June 2012 (26). The cells were maintained in DMEM (Wako Industries) containing 10% FBS (Mediatech), 100 U/mL penicillin/streptomycin, and 2 mmol/L L-glutamine (Mediatech) and grown at 37 C in a 5% CO 2 humidified incubator.…”

Section: Cell Culturementioning

confidence: 99%

Metabolome Analyses Uncovered a Novel Inhibitory Effect of Acyclic Retinoid on Aberrant Lipogenesis in a Mouse Diethylnitrosamine-Induced Hepatic Tumorigenesis Model

Qin¹,

Tatsukawa

Hitomi

et al. 2016

Cancer Prevention Research

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Acyclic retinoid (ACR) is a promising drug under clinical trials for preventing recurrence of hepatocellular carcinoma. The objective of this study was to gain insights into molecular basis of the antitumorigenic action of ACR from a metabolic point of view. To achieve this, comprehensive cationic and lipophilic liver metabolic profiling was performed in mouse diethylnitrosamine (DEN)-induced hepatic tumorigenesis model using both capillary electrophoresis time-of-flight mass spectrometry and liquid chromatography time-of-flight mass spectrometry. ACR significantly counteracted against acceleration of lipogenesis but not glucose metabolism in DEN-treated mice liver, suggesting an important role of lipid metabolic reprogramming in the initiation step of hepatic tumorigenesis. Knowledge-based pathway analysis suggested that inhibition of linoleic acid metabolites such as arachidonic acid, a proinflammatory precursor, played a crucial role in the prevention by ACR of DEN-induced chronic inflammationmediated tumorigenesis of the liver. As a molecular mechanism of the ACR's effect to prevent the aberrant lipogenesis, microarray analysis identified that a key transcription regulator of both embryogenesis and tumorigenesis, COUP transcription factor 2, also known as NR2F2, was associated with the metabolic effect of ACR in human hepatocellular carcinoma cells. Our study provided potential therapeutic targets for the chemoprevention of hepatocellular carcinoma as well as new insights into the mechanisms underlying prevention of hepatic tumorigenesis.

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Section: Cell Culturementioning

confidence: 99%

Metabolome Analyses Uncovered a Novel Inhibitory Effect of Acyclic Retinoid on Aberrant Lipogenesis in a Mouse Diethylnitrosamine-Induced Hepatic Tumorigenesis Model

Qin¹,

Tatsukawa

Hitomi

et al. 2016

Cancer Prevention Research

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“…HepG2 and Huh-7 (26) cells were maintained in Dulbecco's modified Eagle's medium (DMEM) (Nissui Seiyaku, Tokyo, Japan) supplemented with 10% heat-inactivated fetal bovine serum (FBS). The JHH-7 cell line was derived from HBs antigen (HBsAg)-positive hepatocellular carcinoma with liver cirrhosis (10). PLC/PRF/5 cells (Alexander cells) were derived from a primary carcinoma of the liver of an HBsAg-positive patient (2).…”

Section: Cellsmentioning

confidence: 99%

Formation of Vesicular Stomatitis Virus Pseudotypes Bearing Surface Proteins of Hepatitis B Virus

Saha

Tanaka

Jinno-Oue

et al. 2005

J Virol

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Hepatitis B virus (HBV), which belongs to the virus genusHepadnaviridae, is an important etiological agent for acute and chronic hepatitis as well as liver cirrhosis or primary hepatocellular carcinoma (15, 18). The surface proteins of HBV contain three related HBV-encoded glycoprotein species, termed large (L), middle (M), and small (S) proteins (37). As shown in Fig. 1A, all surface proteins are produced from a single open reading frame (ORF) by the use of three different translational start sites that divide this ORF into three domains: preS1, preS2, and S. Translation from the first ATG yields L protein, comprising 390 amino acids (aa), whereas translation from the ATG at aa positions 109 and 164 generates M and S proteins, respectively. The three proteins are posttranslationally modified: each of them exhibits a glycosylation site in the S domain, and an additional glycosylation occurs in the preS2 region of the M protein (Fig. 1A). Either M or S protein, when expressed alone, can be secreted as virus-like particles (25, 45). In contrast, L protein cannot be secreted when expressed alone; instead, it is mainly retained within the endoplasmic reticulum and pre-Golgi regions in the form of intraluminal particles (27,45). It has been reported that the sequence between amino acids 3 and 77 of the preS1 region is necessary for infection of primary human hepatocytes in vitro (21). The preS2 region of M protein has been thought to be involved in polymerized albumin-mediated interaction of HBV (48), but no precise function has yet been definitively assigned to the preS2 region of the M protein. Kann et al. (18) proposed that in association with the preS1 domain of L protein, the preS2 domain of M protein might have a supportive function in viral attachment. Thus, it is still necessary to study the roles of all three proteins in the HBV infection process to clarify the process of entry of HBV into cells.Analysis of HBV infection in vitro has still been difficult due to the lack of a suitable culture system, i.e., lack of susceptible cell lines or of cells producing HBV abundantly. Most in vitro studies have used concentrated, whole virions or human serum samples as virus sources and primary human hepatocytes or human liver cell lines, e.g., HepG2, HuH7, and PH5CH8, as target cells (12,13,21,31,41). However, their infectivities are not so high, and human serum samples and human hepatocytes are not readily available. Despite these difficulties, infection of cells with viral inocula or transfection of cells with HBV DNA has been employed in order to analyze HBV infection in vitro (12,14,46). In vitro infection of human hepatoma (HepG2) cells with hepatitis B virus obtained from the serum of a chronic HBV patient was first reported by Bchini et al. (3).There seems to be only one report that describes an HBV pseudotype: murine leukemia virus (MLV) pseudotype, expected to bear the L and S proteins of HBV (41). The reported MLV(HBV) pseudotype, which was prepared after cotransfection of 293T cells with plasmids expressing...

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“…For this reason, to acquire further insight into the molecular mechanisms of HCC, we performed a systematic functional genomic approach to investigate human HuH-7 and JHH-6 HCC cells. The former are considered an acceptable model for differentiated HCC, whereas the latter are models for undifferentiated, more malignant liver cancer (6)(7)(8)(9)(10). With this approach and the subsequent gene expression analysis on human HCC specimens, we identified an HCC molecular signature consisting of 11 genes that may play important roles in hepatocarcinogenesis.…”

Section: Introductionmentioning

confidence: 99%

Galectin-1 and Its Involvement in Hepatocellular Carcinoma Aggressiveness

Spano

Russo

Maso

et al. 2009

Mol Med

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Hepatocellular carcinoma is one of the most common cancers worldwide. Despite several efforts to elucidate hepatocellular carcinoma molecular pathogenesis, it is still not fully understood. To acquire further insights into the molecular mechanisms of hepatocellular carcinoma, we performed a systematic functional genomic approach on human HuH-7 and JHH-6 cells. The subsequent analysis of the differentially expressed genes in human specimens revealed a molecular signature of 11 genes from which we selected the LGALS1 gene, which was overexpressed in hepatocellular carcinoma. The expression analysis in humans of Galectin-1 (Gal-1), the protein encoded by LGALS1, showed a Gal-1 preferential accumulation in the stromal tissue around hepatocellular carcinoma tumors. Moreover, a significant association between increased expression of Gal-1 in hepatocellular carcinoma and the presence of metastasis was observed. Interestingly, Gal-1 overexpression resulted in an increase of cell migration and invasion. In conclusion, this study provides a portfolio of targets useful for future investigations into molecular marker-discovery studies on a large number of patients and functional assays. In addition, our data provide evidence that Gal-1 plays a role in hepatocellular carcinoma cell migration and invasion, and we suggest that further studies should be conducted to fully establish the role of Gal-1 in hepatocellular carcinoma pathogenesis and evaluate Gal-1 as a potential molecular therapeutic target.

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The search for the hepatitis B virus genome in cells of human hepatocellular carcinoma cell lines.

Cited by 38 publications

References 0 publications

Metabolome Analyses Uncovered a Novel Inhibitory Effect of Acyclic Retinoid on Aberrant Lipogenesis in a Mouse Diethylnitrosamine-Induced Hepatic Tumorigenesis Model

Metabolome Analyses Uncovered a Novel Inhibitory Effect of Acyclic Retinoid on Aberrant Lipogenesis in a Mouse Diethylnitrosamine-Induced Hepatic Tumorigenesis Model

Formation of Vesicular Stomatitis Virus Pseudotypes Bearing Surface Proteins of Hepatitis B Virus

Galectin-1 and Its Involvement in Hepatocellular Carcinoma Aggressiveness

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