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hepatitis b/hypoxia
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[Expressions of hepatitis B virus x protein and hypoxia-inducible factor-1alpha in hepatocellular carcinoma and their possible relationships].
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OBJECTIVE
To investigate the expressions of hepatitis B virus x protein (HBx) and hypoxia-inducible factor-1alpha (HIF-1alpha) in hepatocellular carcinoma (HCC) tissues and HepG2 cells under normoxic and hypoxic conditions.
METHODS
Immunohistochemistry was used to detect the expressions of HBx and
[Hepatitis B x protein activated vascular endothelial growth factor expression through hypoxia inducible factor-1 pathway].
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OBJECTIVE
To investigate whether hepatitis B x protein (HBx) stimulates vascular endothelial growth factor (VEGF) through hypoxia inducible factor-1 (HIF-1 alpha) pathway.
METHODS
Two plasmids including pIRES-EGFP-HBx and pTK-Hyg were co-transfected to a hepatocellular carcinoma cell line SMMC-7721.
Hepatitis B virus induces hypoxia-inducible factor-2α expression through hepatitis B virus X protein.
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A growing number of studies suggest that the hepatitis B virus X protein (HBx) enhances the protein stability of the hypoxia-inducible factor-1α (HIF-1α). However, the relationship between hepatitis B virus (HBV), HBx and hypoxia-inducible factor-2α (HIF-2α) has not yet been fully elucidated.
Role of hypoxia-inducible factor-alpha in hepatitis-B-virus X protein-mediated MDR1 activation.
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The transition from chemotherapy-responsive cancer cells to chemotherapy-resistant cancer cells is mainly accompanied by the increased expression of multi-drug resistance 1 (MDR1). We found that hepatitis-B-virus X protein (HBx) increases the transcriptional activity and protein level of MDR1 in a
Human hepatitis B virus X protein is a possible mediator of hypoxia-induced angiogenesis in hepatocarcinogenesis.
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The hepatitis B virus (HBV)-encoded transcriptional activator HBV-X protein (HBx) was known to be involved in hepatocarcinogenesis. Hepatocarcinogenesis generally included an active angiogenesis that was mainly considered to be due to a local hypoxia in liver tissues. However, the exact mechanisms
Hidden secret in hepatitis B viral X protein mutation and hypoxia-inducible factor-1α in hepatocarcinoma cancer.
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Hepatitis B type virus (HBV) is an old hepato oncogenic and hepatitis agent. Hepatitis B viral X protein (HBx)-induced malignant transformation requires the excess amounts of ATP level, inducing the extremely oxygen-deprived condition in the cancer tissues and vessels. To adapt, cells go to shift
The expression of hypoxia-inducible factor-1alpha in hepatitis B virus-related hepatocellular carcinoma: correlation with patients' prognosis and hepatitis B virus X protein.
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Hypoxia inducible factor-1alpha (HIF-1alpha) was well correlated with carcinogenesis and tumor progression in many kinds of cancer. In this study, high expression of HIF-1alpha was found in 37 of the 72 (51.39%) tumor specimens, and significantly correlated with venous invasion and lymphonode
The carboxy-terminus of the hepatitis B virus X protein is necessary and sufficient for the activation of hypoxia-inducible factor-1alpha.
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Hepatitis B virus X protein (HBx) of the hepatitis B virus is strongly implicated in angiogenesis and metastasis during hepatocarcinogenesis. Previously, we reported that HBx enhances activity of hypoxia-inducible factor-1alpha (HIF-1alpha), a potent transactivator that induces angiogenic factors.
Hypoxia-induced human deoxyribonuclease I is a cellular restriction factor of hepatitis B virus.
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Numerous human APOBEC3 cytidine deaminases have proven to be, inter alia, host cell restriction factors for retroviruses and hepadnaviruses. Although they can bind to genomic RNA and become encapsidated, they are only catalytically active on single-stranded DNA. As there are many cellular
Hepatitis B virus X protein enhances transcriptional activity of hypoxia-inducible factor-1alpha through activation of mitogen-activated protein kinase pathway.
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Hepatitis B virus X protein (HBx) of the hepatitis B virus was strongly implicated in angiogenesis and metastasis during hepatocarcinogenesis. Here, we explored the possibility of cross-talk between HBx and hypoxia-inducible factor-1alpha (HIF-1alpha), a potent transcriptional inducer of angiogenic
Hepatitis B virus X protein and hypoxia‑inducible factor-1α stimulate Notch gene expression in liver cancer cells.
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Increasing evidence has demonstrated that Notch genes, including Notch1, Notch2, Notch3 and Notch4, are involved in carcinogenesis. However, the expression and regulation of Notch genes in hepatocellular carcinoma (HCC) tissues have not been fully investigated. In the present study,
Hepatitis B virus X protein induces the expression of MTA1 and HDAC1, which enhances hypoxia signaling in hepatocellular carcinoma cells.
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Expression level of metastasis-associated protein 1 (MTA1) is closely related to tumor growth and metastasis in various cancers. Although increased expression level of MTA1 was observed in hepatocellular carcinoma (HCC), role of MTA1 complex containing histone deacetylase (HDAC) in hepatitis B virus
Hepatitis B virus X protein induces angiogenesis by stabilizing hypoxia-inducible factor-1alpha.
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Hepatitis B virus X protein (HBx) is closely involved in the development of hepatocellular carcinoma, a highly vascularized solid tumor. Here we show that HBx increases the transcriptional activity and protein level of hypoxia-inducible factor-1alpha (HIF-1alpha) under both normoxic and hypoxic
Association between hypoxia-inducible factor-1α gene polymorphisms and risk of chronic hepatitis B and hepatitis B virus-related liver cirrhosis in a Chinese population: a retrospective case-control study.
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BACKGROUND
Our recent study demonstrated a significant association between HIF-1α polymorphisms and hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC). Since chronic hepatitis B (CHB), liver cirrhosis (LC), and HCC are progressive stages of chronic HBV infection, the aim of this study is
[Expression and clinical significance of hypoxia-inducible factor-1 in liver tissue of patients with chronic hepatitis B in highland and plain areas].
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