hepatoblastoma/hypoxia

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Enhanced erythropoietin secretion in hepatoblastoma cells in response to hypoxia.

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Erythropoietin (Ep) levels in spent culture media of a Hep G2 human hepatoblastoma cell line were measured by radioimmunoassay (RIA), fetal mouse liver erythroid colony formation (FMLC), and the exhypoxic polycythemic mouse assay (EHPCMA). The Hep G2 cells at high density produced approximately 700

Regulation of erythropoietin production in a human hepatoblastoma cell line.

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Production of immuno and biologically active erythropoietin was documented to occur in the human hepatoblastoma cell line HepG-2. The expression of the erythropoietin gene was further verified by Northern blot analysis using a single stranded RNA probe. In vitro studies showed that erythropoietin

Hypoxia up-regulates the activity of a novel erythropoietin mRNA binding protein.

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The mechanisms which control the production of erythropoietin (Epo) remain enigmatic. Recent data suggest that the half-time of Epo messenger RNA (mRNA) is increased by hypoxia in Hep 3B cells, a human hepatoma line. The post-transcriptional regulation of other rapidly degraded mRNAs is mediated by

Cell selective induction and transcriptional activation of immediate early genes by hypoxia.

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c-fos and jun belong to the immediate early response genes (IERG) that initiate phenotypic changes in response to a variety of extracellular stimuli. In the present study, we examined whether hypoxia induces IERG expression in isolated cells. Experiments were performed on pheochromocytoma-12

Metformin attenuates hypoxia-induced resistance to cisplatin in the HepG2 cell line.

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Hepatoblastoma is the most commonly occurring liver tumor in children. Preoperative chemotherapy and surgery have improved treatment outcomes; however, further improvements are required in the treatment of advanced cases. Recently, the efficacy of transarterial chemoembolization (TACE) has garnered

Phosphorylation of c-Jun N-terminal kinase in human hepatoblastoma cells is transiently increased by cold exposure and further enhanced by subsequent warm incubation of the cells.

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During a cold preservation and reperfusion process of organs, cells are exposed to two major stresses, i.e. changes in oxygen concentration and temperature. c-Jun N-terminal kinase (JNK) /stress-activated protein kinase is activated by various stresses through its phosphorylation. Although hypoxia

Molecular biology of circulatory shock. Part III. Human hepatoblastoma (HepG2) cells demonstrate two patterns of shock-induced gene expression that are independent, exclusive, and prioritized.

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During shock and resuscitation, parenchymal cells of solid organs are exposed to a rapidly changing microenvironment, which may include a reduced oxygen tension and an increased concentration of certain cytokines including tumor necrosis factor alpha and interleukin-1. In vivo experiments that

Hypoxia-activated metabolic pathway stimulates phosphorylation of p300 and CBP in oxygen-sensitive cells.

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Transcription co-activators and histone acetyltransferases, p300 and cyclic AMP responsive element-binding protein-binding protein (CBP), participate in hypoxic activation of hypoxia-inducible genes. Here, we show that exposure of PC12 and cells to 1-10% oxygen results in hyperphosphorylation of

Hypoxia induces the expression of TET enzymes in HepG2 cells.

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Hypoxia promotes tumor malignancy in solid tumors. One key mechanism by which this occurs is via epigenetic alteration. The present study demonstrates that hypoxia upregulates the expression of the ten-eleven-translocation 5-methylcytosine dioxygenase (TET) enzymes, which catalyze the conversion of

H19 suppresses the growth of hepatoblastoma cells by promoting their apoptosis via the signaling pathways of miR-675/FADD and miR-138/PTK2.

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BACKGROUND The objective of this study was to clarify the molecular pathways involved in hepatitis B virus (HBV)-induced hepatoblastoma. METHODS The expression of factors in different signaling pathways (H19, miR-675, miR-138, protein tyrosine kinase 2 [PTK2], fas-associated death domain [FADD],

Up-regulation of breast cancer resistance protein expression in hepatoblastoma following chemotherapy: A study in patients and in vitro.

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OBJECTIVE Hepatoblastoma (HB), the most common pediatric malignant liver tumor, is treated with chemotherapy to facilitate surgical resection. Previous studies suggest that HB acquires chemoresistance via increased expression of multidrug resistance protein 1 (MDR1, ABCC1). There is no well

Redox mechanisms switch on hypoxia-dependent epithelial-mesenchymal transition in cancer cells.

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Epithelial-mesenchymal transition (EMT) and hypoxia are considered as crucial events favouring invasion and metastasis of many cancer cells. In this study, different human neoplastic cell lines of epithelial origin were exposed to hypoxic conditions in order to investigate whether hypoxia per se may

The effect of OP 2507, a stable analogue of prostacyclin, on Hep G2 exposed to hypoxia.

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We developed a model for screening drugs to reduce ischemic liver damage using Hep G2, a hepatoblastoma cell line, and examined the effect of OP 2507, a stable analogue of prostacyclin, on hypoxic cell damage. Hypoxic exposure of the cells was done for 16 hr in an air-tight chamber which was placed

Effects of transient overexpression or knockdown of cytochrome P450 reductase on reactive oxygen species generation and hypoxia reoxygenation injury in liver cells.

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1. Literature data suggest that the electron-donating enzyme, cytochrome P450 reductase (CPR), might act as a source of reactive oxygen species (ROS). However, the role of CPR in pathophysiological conditions associated with oxidative stress is unknown. The aim of the present study was to study the

Congenital Extrahepatic Portosystemic Shunt (Abernethy Malformation Type Ib) with Associated Hepatocellular Carcinoma: Case report and Literature Review.

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Abernethy malformation, also termed congenital portosystemic shunt and congenital absence of portal vein (CAPV) is the result of malformation of the splanchnic venous system. Congenital portosystemic shunts are divided into extra-and intrahepatic shunts. Two shunts have been defined: type I is

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