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The role of a novel CAR-induced gene TUBA8 in hepatocellular carcinoma cell lines

ABSTRACT: The Tuba8 gene was identified as a CAR-regulated gene that was induced during phenobarbital (PB) promotion of liver tumor. TUBA8 was then over-expressed in heaptocarcinoma cells to determine the function of TUBA8.

ORGANISM(S): Mus musculus

PROVIDER: GSE29108 | GEO | 2011/11/29

SECONDARY ACCESSION(S): PRJNA140371

REPOSITORIES: GEO

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The role of a novel CAR-induced gene TUBA8 in hepatocellular carcinoma cell lines

Project description:The Tuba8 gene was identified as a CAR-regulated gene that was induced during phenobarbital (PB) promotion of liver tumor. TUBA8 was then over-expressed in heaptocarcinoma cells to determine the function of TUBA8. First, identify genes that are regulated by CAR and are induced during liver tumor development. Second, overexpressiong of an identified gene in transformed cells to detemine the biolgical function of the gene product. In this manuscript, the TUBA8 gene was examined.

2011-11-29 | E-GEOD-29108 | biostudies-arrayexpress

Effect of phenobarbital on CAR and PXR regulated genes involved in drug metabolism and cholesterol homeostasis

Project description:The nuclear receptors CAR (constitutive androstane receptor) and PXR (pregnane X receptor) mediate the effects of phenobarbital (PB) on gene transcription. To investigate the relative role of CAR and PXR in the induction response, cDNA arrays were generated containing 120 genes which are known to be regulated with these or related nuclear receptors (genes involved in drug metabolism, cholesterol biosynthesis, sterol synthesis/transport, heme synthesis). Samples from livers of wild type and CAR-/-, PXR-/- or CAR/PXR-/- knockout mice were tested after treatment with PB for gene expression within the European Framework V program “Steroltalk” (www.steroltalk.net). Results from these experiments unexpectedly revealed that if CAR and PXR are deleted, PB increases the expression of several other nuclear receptors and genes involved in drug metabolism and cholesterol biosynthesis. Animals were injected i.p. 100mg/kg phenobarbital or vehicle (5% DMSO in corn oil). After 12h they were sacrificed and total RNA was isolated from the livers. Pools of untreated samples were mixed in each genetic variant group (wild type and CAR-/-, PXR-/- or CAR/PXR-/-) with the phenobarbital treated ones and hybridized to Sterolgene V1 arrays.

2008-08-23 | E-GEOD-12489 | biostudies-arrayexpress

Dose-response modeling of early molecular and cellular key events in CAR-mediated hepatocarcinogenesis pathway

Project description:Male and female CD-1 mice were administered dietary Phenobarbital for 2 or 7 days. In-life, enzyme activity, cell proliferation, genomic analysis, and Bench-mark dose modeling was carried out. The goal was to exmaine low-dose PB effects on early key events in CAR-mediated hepatocarcinogenesis. PB at 0, 0.15, 1.5, 15, 75, or 150 mg/kg-day for 2 or 7 days to characterize multiple apical and molecular endpoints.

2014-02-01 | E-GEOD-54597 | biostudies-arrayexpress

Effect of phenobarbital on CAR and PXR regulated genes involved in drug metabolism and cholesterol homeostasis

2008-08-23 | GSE12489 | GEO

Transcriptional profiling of Primary Human Hepatocytes (PHH) depleted for CAR and treated with CITCO or Phenobarbital in -/+EGF medium

Project description:In primary human hepatocytes (PHH) the involvement of the Constitutive Androstane Receptor (CAR) in genes regulations has never been evaluated at the transcriptomic level. Here we investigated the impact of CAR depletion and epidermal growth factor on CAR dependent gene modulation in PHH. The xenosensor was activated by its direct (CITCO) or indirect (Phenobarbital/PB) agonists in presence or in absence of EGF.

2018-04-27 | GSE68493 | GEO

Role of a novel CAR-induced gene, TUBA8, in hepatocellular carcinoma cell lines.

Project description: Not available

| S-EPMC3178051 | biostudies-literature

Dose-response modeling of early molecular and cellular key events in CAR-mediated hepatocarcinogenesis pathway

2014-02-01 | GSE54597 | GEO

Comparison of the hepatic effects of phenobarbital in chimeric mice containing either rat or human hepatocytes with humanized constitutive androstane receptor (CAR) and pregnane X receptor (PXR) mice (hCAR/hPXR mice) [rat liver experiments]

Project description:Using a chimeric mouse humanized liver model, we provided evidence that human hepatocytes are refractory to the mitogenic effects of rodent constitutive androstane receptor (CAR) activators. To evaluate the functional reliability of this model, the present study examined mitogenic responses to phenobarbital (PB) in chimeric mice transplanted with rat hepatocytes, since rats are responsive to CAR activators. Treatment with 1000 ppm PB for 7 days significantly increased replicative DNA synthesis (RDS) in rat hepatocytes of the chimeric mice, demonstrating that the transplanted hepatocyte model is functionally reliable for cell proliferation analysis. Treatment of humanized CAR and pregnane X receptor (PXR) mice (hCAR/hPXR mice) with 1000 ppm PB for 7 days significantly increased hepatocyte RDS together with increases in several mitogenic genes. Global gene expression analysis was performed with liver samples from this and from previous studies focusing on PB-induced Wnt/β-catenin signaling, and showed that altered genes in hCAR/hPXR mice clustered most closely with liver tumor samples from a diethylnitrosamine/PB initiation/promotion study than with wild type mice. However, different gene clusters were observed for chimeric mice with human hepatocytes for Wnt/ß-catenin signaling when compared to those of hCAR/hPXR mice, wild type mice and liver tumor samples. The results of this study demonstrate clear differences in the effects of PB on hepatocyte RDS and global gene expression between human hepatocytes of chimeric mice and hCAR/hPXR mice, suggesting that the chimeric mouse model is relevant to humans for studies on the hepatic effects of rodent CAR activators, whereas the hCAR/hPXR mouse is not.

2021-04-20 | GSE149230 | GEO

2021-04-20 | GSE149229 | GEO

2021-04-20 | GSE149228 | GEO

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