Cytokine regulation of HIV-1 LTR transactivation in human hepatocellular carcinoma cell lines

Hsu, Mei‐Ling; Chen, Shiuhwei; Lin, Kwang‐Huei; Liao, Shun-Kuei; Chang, Kenneth S. S.

doi:10.1016/0304-3835(95)03820-m

Cited by 10 publications

(6 citation statements)

References 26 publications

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“…Whereas in human macrophages, IFN-g was found to exhibit an inhibitory effect, 48 in human hepatoma cells, it has been demonstrated to have an enhancing effect. 49 Our results thus add further credence to the concept that the effect of IFN-g is not pleiotropic and is determined by cell-specific transcriptional mechanisms.…”

Section: Figsupporting

confidence: 74%

Role of Placental Cytokines in Transcriptional Modulation of HIV Type 1 in the Isolated Villous Trophoblast

Zachar

Fink

Koppelhus

et al. 2002

AIDS Research and Human Retroviruses

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During pregnancy, a complex cytokine network is present at the maternal-fetal interface in order to support normal growth and development of the placenta and fetus. HIV can frequently infect placental trophoblast but the impact of cytokines produced locally by the placenta and decidua on virus expression and replication is unknown. We comprehensively assayed the cytokines typically present in the placental microenvironment for their potential to modulate HIV transcriptional activation in the isolated trophoblast cells employing a transient transfection assay with luciferase as a reporter gene. Long terminal repeats (LTRs) of two divergent virus strains, HIV-1 LAI and HIV-1 NDK, were used to analyze virus-specific features. Four cytokines, epidermal growth factor (EGF), granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin 1 beta (IL-1 beta), and tumor necrosis factor alpha (TNF-alpha), were found to stimulate promoters of both viruses, whereas interferon alpha (IFN-alpha) and IFN-beta were found to suppress the transcription driven from both promoters. The differences observed between the two viruses did not reach a statistically significant level. None of the remaining cytokines, including EGF; GM-CSF; insulin-like growth factor I (IGF-I); IFN-alpha, IFN-beta, and IFN-gamma; IL-1 alpha, IL-1 beta, IL-2, IL-6, and IL-10; leukemia inhibitory factor (LIF); macrophage colony-stimulating factor (M-CSF); platelet-derived growth factor BB (PDGF-BB); transforming growth factor beta (TGF-beta); and TNF-alpha, affected transcriptional expression of the promoter constructs. Our results demonstrate that the local balance of cytokines may be critical for activation of HIV in the syncytiotrophoblast-cytotrophoblast layer and thus play an important role in the transmission of virus across the placental barrier.

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Section: Figsupporting

confidence: 74%

Role of Placental Cytokines in Transcriptional Modulation of HIV Type 1 in the Isolated Villous Trophoblast

Zachar

Fink

Koppelhus

et al. 2002

AIDS Research and Human Retroviruses

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“…Subsequent immunohistochemistry and in situ hybridization studies using liver specimens from HIV-infected patients have demonstrated HIV p24 protein and HIV RNA in Kupffer cells, inflammatory mononuclear cells, sinusoidal cells, intrahepatic lymphocytes, and/or hepatocytes [28,31-35]. Efficient activation of the HIV long terminal repeat also occurs in hepatocytes [36-38]. HIV compartmentalization in the liver has also been reported recently, suggesting that viral adaptation for replication within the liver may occur in vivo [30].…”

Section: Discussionmentioning

confidence: 99%

Low-level HIV infection of hepatocytes

Kong

Maya

Moreno‐Fernandez

et al. 2012

Virol J

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BackgroundThere are only limited data on whether HIV infection occurs within the liver; therefore, we explored early and late stages of the HIV life cycle in two hepatocyte cell lines – Huh7.5 and Huh7.5JFH1 – as well as in primary human hepatocytes.ResultsIntegrated HIV DNA was detected in Huh7.5 and Huh7.5JFH1 cells, as well as in primary hepatocytes, and was inhibited by the integrase inhibitor raltegravir in a dose-dependent manner. HIV p24 protein was also detected in cell culture supernatants at days 1, 3, 5, and 7 post-infection and was inhibited by AZT, although levels were modest compared to those in a lymphocyte cell line. Culture supernatants from HIV-infected hepatocytes were capable of infecting a non-hepatic HIV indicator cell line.ConclusionsThese results indicating low-level HIV replication in hepatoctyes in vitro complement evidence suggesting that HIV has deleterious effects on the liver in vivo.

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“…HepG2, Hep3B, and SK-Hep–1 cells were purchased from ATCC. HepJ5 and Mahlavu cell were gifted from Dr. C.S Yang, National Taiwan University and Dr. C. P. Hu, Veterans General Hospital, Taiwan [ 17 , 18 ]. Those cells were cultured in Dulbecco’s modified Eagle medium (DMEM) (Sigma Chemical Co., St. Louis.…”

Section: Methodsmentioning

confidence: 99%

Proteomic Characterization of Annexin l (ANX1) and Heat Shock Protein 27 (HSP27) as Biomarkers for Invasive Hepatocellular Carcinoma Cells

et al. 2015

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To search for reliable biomarkers and drug targets for management of hepatocellular carcinoma (HCC), we performed a global proteomic analysis of a pair of HCC cell lines with distinct differentiation statuses using 2-DE coupled with MALDI-TOF MS. In total, 106 and 55 proteins were successfully identified from the total cell lysate and the cytosolic, nuclear and membrane fractions in well-differentiated (HepG2) and poorly differentiated (SK-Hep–1) HCC clonal variants, respectively. Among these proteins, nine spots corresponding to proteins differentially expressed between HCC cell types were selected and confirmed by immunofluorescence staining and western blotting. Notably, Annexin 1 (ANX1), ANX–2, vimentin and stress-associated proteins, such as GRP78, HSP75, HSC–70, protein disulfide isomerase (PDI), and heat shock protein–27 (HSP27), were exclusively up-regulated in SK-Hep–1 cells. Elevated levels of ANX–4 and antioxidant/metabolic enzymes, such as MnSOD, peroxiredoxin, NADP-dependent isocitrate dehydrogenase, α-enolase and UDP-glucose dehydrogenase, were observed in HepG2 cells. We functionally demonstrated that ANX1 and HSP27 were abundantly overexpressed only in highly invasive types of HCC cells, such as Mahlavu and SK-Hep–1. Knockdown of ANX1 or HSP27 in HCC cells resulted in a severe reduction in cell migration. The in-vitro observations of ANX1 and HSP27 expressions in HCC sample was demonstrated by immunohistochemical stains performed on HCC tissue microarrays. Poorly differentiated HCC tended to have stronger ANX1 and HSP27 expressions than well-differentiated or moderately differentiated HCC. Collectively, our findings suggest that ANX1 and HSP27 are two novel biomarkers for predicting invasive HCC phenotypes and could serve as potential treatment targets.

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Cytokine regulation of HIV-1 LTR transactivation in human hepatocellular carcinoma cell lines

Cited by 10 publications

References 26 publications

Role of Placental Cytokines in Transcriptional Modulation of HIV Type 1 in the Isolated Villous Trophoblast

Role of Placental Cytokines in Transcriptional Modulation of HIV Type 1 in the Isolated Villous Trophoblast

Low-level HIV infection of hepatocytes

Proteomic Characterization of Annexin l (ANX1) and Heat Shock Protein 27 (HSP27) as Biomarkers for Invasive Hepatocellular Carcinoma Cells

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