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HNF4α and TCF4 (TCF7L2) ChIPseq in Tet-On HCT116 inducible cell lines that express either the human HNF4α2 or HNF4α8 under the control of doxycycline (DOX) [ChIP-Seq]

ABSTRACT: Purpose: Aim of the study is to determine how many of the dysregulated genes in the RNAseq are direct targets of (P1) HNF4α2 and (P2) HNF4α8 and examine HNF4α and TCF4 binding in vivo. We performed ChIPseq on TCF4 in the absense or presence of DOX in the Tet-On inducible HCT116 HNF4α2 and HNF4α8 lines, and ChIPseq for HNF4α (a445 Ab) in the presence of DOX. Methods: HNF4α2 and HNF4α8 lines were induced with 0.3 μg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the NEXTflex ChIPseq. Result: There were more HNF4α2 peaks than HNF4α8 peaks, with some common peaks bound by HNF4α2 and HNF4α8. Binding patterns were observed between HNF4α and TCF4. Conclusion: HNF4α2 can displace TCF4 better than HNF4α8 on AP-1 bound sites. Tet-On inducible HCT116 cell (HNF4α2 and HNF4α8) lines, treated with (0.3 μg/mL) or without DOX for 24 hours, were 50bp single-end sequenced using Illumina-compatible-NEXTflex ChIP kit (Bioo Scientific).

ORGANISM(S): Homo sapiens

SUBMITTER: joseph dhahbi

PROVIDER: E-GEOD-62890 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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HNF4α and TCF4 (TCF7L2) ChIPseq in Tet-On HCT116 inducible cell lines that express either the human HNF4α2 or HNF4α8 under the control of doxycycline (DOX) [ChIP-Seq]

Project description:Purpose: Aim of the study is to determine how many of the dysregulated genes in the RNAseq are direct targets of (P1) HNF4α2 and (P2) HNF4α8 and examine HNF4α and TCF4 binding in vivo. We performed ChIPseq on TCF4 in the absense or presence of DOX in the Tet-On inducible HCT116 HNF4α2 and HNF4α8 lines, and ChIPseq for HNF4α (a445 Ab) in the presence of DOX. Methods: HNF4α2 and HNF4α8 lines were induced with 0.3 μg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the NEXTflex ChIPseq. Result: There were more HNF4α2 peaks than HNF4α8 peaks, with some common peaks bound by HNF4α2 and HNF4α8. Binding patterns were observed between HNF4α and TCF4. Conclusion: HNF4α2 can displace TCF4 better than HNF4α8 on AP-1 bound sites.

2015-08-28 | GSE62890 | GEO

Genome-wide expression profile of the Tet-On HCT116 inducible cell line that express either the human HNF4α2 or HNF4α8 under control of Doxycycline (DOX) [RNAseq]

Project description:Purpose: Aim of the study is to identify functional differences between the P1 and P2-HNF4α isoforms. To do this, we generated Tet-On inducible lines that express either the human (P1) HNF4α2 or (P2) HNF4α8 under control of DOX in the HCT116 human colon cancer cells. Methods: HNF4α2 and Parental lines were induced with 0.3 μg/mL DOX, while HNF4α8 line was induced with either 0.1 or 0.3 μg/mL DOX for 24 hours. Samples were generated by deep sequencing, using the Illumina TruSeq RNA. Result: There were common and unique dysregulated genes identified in the HNF4α2 and HNF4α8 lines (+DOX); more upregulated genes than downregulated genes in both the lines. Conclusion: The functional difference between HNF4α2 and HNF4α8 is that the latter tends to upregulate genes involved in proliferation and anti-apoptosis while HNF4α2 upregulates genes involved in growth suppression and cell death. Tet-On inducible HCT116 cell (Parental, HNF4α2, and HNF4α8) lines, treated with (0.0, 0.1, or 0.3 μg/mL) DOX for 24 hours, were 50bp pair-ended sequenced in triplicate using Illumina TruSeq RNA Sample Prep v2 Kit.

2015-08-28 | E-GEOD-62889 | biostudies-arrayexpress

Genome-wide expression profile of the Tet-On HCT116 inducible cell line that express either the human HNF4α2 or HNF4α8 under control of Doxycycline (DOX) [RNAseq]

2015-08-28 | GSE62889 | GEO

T-cell factor 4 and β-catenin chromatin occupancies pattern zonal liver metabolism.

Project description:β-catenin signaling can be both a physiological and an oncogenic pathway in the liver. It controls compartmentalized gene expression, allowing the liver to ensure its essential metabolic function. It is activated by mutations in 20 to 40% of hepatocellular carcinomas with specific metabolic features. We decipher the molecular determinants of β-catenin-dependent zonal transcription using mice with β-catenin-activated or -inactivated hepatocytes, characterizing in vivo their chromatin occupancy by Tcf4 and β-catenin, their transcriptome and their metabolome. We find that Tcf4 DNA-bindings depend on β-catenin. Tcf4/β-catenin binds Wnt-responsive elements preferentially around β-catenin-induced genes. In contrast, genes repressed by β-catenin bind Tcf4 on Hnf4-responsive elements. β-catenin, Tcf4 and Hnf4α interact, dictating β-catenin transcription which is antagonistic to that elicited by Hnf4α. Finally, we find the drug/bile metabolism pathway to be the one most heavily targeted by β-catenin, partly through xenobiotic nuclear receptors. We conclude that β-catenin patterns the zonal liver together with Tcf4, Hnf4α and xenobiotic nuclear receptors. This network represses lipid metabolism, and exacerbates glutamine, drug and bile metabolism, mirroring hepatocellular carcinomas with β-catenin mutational activation. In vivo liver samples in 4 conditions: Betacat activated (WCE, Tcf4 chipseq, Betacat chipseq, mRNAseq with 2 replicates), Betacat null (WCE, Tcf4 chipseq, mRNAseq with 2 replicates), Betacat control (mRNAseq with 2 replicates), Wild type (mRNAseq with 2 replicates)

2014-01-18 | E-GEOD-35213 | biostudies-arrayexpress

Homo sapiens

Project description:HNF4α and TCF4 (TCF7L2) ChIPseq in Tet-On HCT116 inducible cell lines that express either the human HNF4α2 or HNF4α8 under the control of doxycycline (DOX) [ChIP-Seq]

| PRJNA265991 | ENA

T-cell factor 4 and β-catenin chromatin occupancies pattern zonal liver metabolism.

2014-01-18 | GSE35213 | GEO

Progression of liver tumor was promoted by tris(1,3-dichloro-2-propyl)phosphate through the induction of inflammatory responses in krasV12 transgenic zebrafish

Project description:In this study, krasV12 genetically modified zebrafish, Tg(fabp10:rtTA2s-M2; TRE2:EGFP-krasG12V), an inducible liver tumor model, was used to evaluate the promotion potential of TDCIPP for liver tumor. Briefly, krasV12 transgenic females were exposed to 0.3 mg/L TDCIPP, 20 mg/L doxycycline (DOX) and a binary mixture of 0.3 mg/L TDCIPP with 20 mg/L DOX, and liver size, histopathology, and transcriptional profiles of liver were tested. Treatment with TDCIPP increased the liver size and caused more aggressive hepatocellular carcinoma (HCC). Furthermore, compared with the exposure to DOX, TDCIPP in the presence of DOX up-regulated the expression of genes relevant with salmonella infection and the toll-like receptor signaling pathway, implying an occurrence of inflammatory reaction, which was sustained by the increase in the amount of infiltrated neutrophils in the liver of Tg(lyz:DsRed2) transgenic zebrafish larvae. Collectively, our results suggested that TDCIPP could promote the liver tumor progression by induction of hepatic inflammatory responses.

2019-06-21 | GSE133076 | GEO

Liver-specific matrin-3 knockout alters the chromatin accessibility in the liver of mice [ATAC-seq]

Project description:Matrin-3 is an RNA-binding protein involved in the pathogenesis of human diseases. Here we examined its previously uncharacterized role in regulating chromatin accessibility in the liver of mice. Bulk ATAC-seq and bioinformatics analysis identified 523 and 829 differential peaks (FDR < 0.05), respectively, in the liver of female mice fed a chow diet or 60% HFD for 16 weeks. Peak annotation by HOMER and ChIPseeker identified 183 and 444 genes, respectively, that are associated with the differential peaks. Enrichr analysis of these genes revealed that Hallmark terms such as "Xenobiotic metabolism" was enriched in the liver of chow-fed and HFD-fed mice. TRRUST database analysis from Metascape uncovered that Hnf4α is the main transcription factor regulating these peak-associated genes in the liver of chow-fed mice, and Hnf4α and Nr1i3 are the main transcription factors regulating these peak-associated genes in the liver of HFD-fed mice. Our data demonstrated that liver-specific matrin-3 deficiency alters chromatin accessibility likely affecting the action of two transcription factors Hnf4α and Nr1i3 in the liver of mice.

2024-10-01 | GSE246704 | GEO

Next-generation sequencing facilitates quantitative analysis of miRNAs of cetuximab-resistant colorectal cancer (HCT116-R) cells

Project description:Total RNAs were isolated from three groups, including A group (0×10^9/mL PA-MSHA-treated HCT116 cells), B group (0.3×10^9/mL PA-MSHA-treated HCT116 cells) and C group (0.4×10^9/mL PA-MSHA-treated HCT116 cells). MiRNA sequencing was performed to assess differential expression using next-generation sequencing. The data showed that most miRNAs levels were different in A, B and C groups. Importantly, miR-7-5p was greatly increased in a dose-dependent manner.

2021-08-13 | GSE181843 | GEO

Differential Genomic Effects of Six Different Nanomaterials on Human Liver HepG2 Cells

Project description:Human Hepatocellular Carcinoma cells (HepG2) were exposed to six nanomaterials containing either Cerium oxide (CeO2) or Titanium oxide (TiO2) nanoparticles. Three different concentrations were tested: 0.3, 3, or 30 μg/mL) for 3 days. Microarray analysis was performed to identify genes differentially expressed following exposure to these chemicals.

2018-08-28 | GSE117056 | GEO

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