HT-29 cells treated with IFN-γ
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE38516 | GEO | 2013/08/06
SECONDARY ACCESSION(S): PRJNA168027
REPOSITORIES: GEO
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Project description:Expression data from HT-29 human colon adenocarcinoma cells treated with IFN-γ for 24 hr Total RNA was isolated from HT-29 cells after 24h stimulation with 200 U ml-1 IFN-γ (Roche). The experiment was done on three biological replicates.
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Project description:DNase-seq on immortalized cell line HT-29, epithelial cells from a 44 year old female adult human colon with a colorectal adenocarcinoma. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODE_Data_Use_Policy_for_External_Users_03-07-14.pdf
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Project description:RNA-seq data from HT-29 cells treated with IFN-M-NM-3 for 24 hr, MCF10A cells, and MDA-MB-436 cells. mRNA profiles of HT-29, MCF10A, and MDA-MB-436 were generated by deep sequencing using Illumina HiSeq 2000. All RNA sequencing data was generated by the Genomics Services Lab at the HudsonAlpha Institute for Biotechnology (Huntsville, AL).
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Project description:Expression data from HT-29 cells treated with IFN-γ for 24 hr, MCF10A cells, and MDA-MB-436 cells. Total RNA was isolated with the RNeasy Mini Kit (Qiagen). Sense-strand cDNA synthesis, terminal labeling, and hybridization were performed using Ambion WT Expression Kit (Applied Biosystems, P/N 4425209).
2013-08-06 | E-GEOD-45195 | biostudies-arrayexpress
Project description:The goal of this study is to use RNA-sequencing to profile the transcriptional changes in HT-29 cells with ING3 deficiency. Specifically, we were interested in determining the IFN and ISGs in response to ING3 KO. Several ISGs including IFI44L and IFITM1 were up-regulated in ING3 KO HT-29 cells, indicating that the broad resistance to virus infection in ING3 KO cells were mediated by heightened IFN and ISG responses.
2021-08-04 | GSE166219 | GEO
Project description:Transcriptional profiling of HT-29 human colon cancer cells transfected with non-targeting control (NTC) siRNA and two different siRNA sequences against CDK8 (siCDK8-1 and siCDK8-2).
2012-03-05 | GSE30815 | GEO
Project description:Purpose: Identify genes regulated by GPR126 in colon cancer cells by RNA-seq analysis Methods: Use shRNAs to knock down GPR126 in HT-29 cells, total RNAs from scramble group (NC) and GPR126 knockdown group (Sh1) were subjected to RNA-sequencing. Results: Around 700 transcriptomes were up-regulated in GPR126 knockdown HT-29 cells, and 14000 transcriptomes were down-regulated in GPR126 knockdown HT-29 cells.GPR126 mainly regualtes genes from DNA synthesis and cell cycle-related pathways. Conclusions: Our study firstly showed the function of GPR126 regulating colon cancer cell proliferation by targeting genes invovled in DNA synthesis and cell cycle-related pathways.
2017-11-09 | GSE106696 | GEO
Project description:Low intracellular folate levels diminish the growth rate of HT-29 human colon cancer cells. This is accompanied by a metabolic shift from cytosolic glycolysis towards mitochondrial oxidative phosphorylation, as demonstrated by a lower lactate production and an increased mitochondrial oxygen consumption rate. To obtain insight in the molecular effects underlying these changes, the steady state gene expression profiles of HT-29 cells with different intracellular folate concentrations were compared. The gene expression profile of HT-29 cells with low intracellular folate levels (grown for 3 weeks in 10 ng/ml folic acid (PGA)) was clearly distinct from that of the other exposure conditions, which provide sufficient intracellular folate levels (100 ng/ml PGA, 10 ng/ml methyltetrahydrofolate (MTHF) or 100 ng/ml MTHF). Intracellular folate deficiency, contrary to expectation, did not lead to major changes in expression of genes involved in energy metabolism. This suggests that the shift towards mitochondrial oxidative phosphorylation is not mediated at the transcription level. Furthermore, only minor changes in the expression of folate metabolism related genes were observed. The changes that were observed were consistent with nucleotide salvage and in agreement with nucleotide need of the slow-growing folate-deficient HT-29 cells. The major observed effects were on cell cycle related gene expression, which was increased and interferon-responsive gene expression, which was reduced. The increase in cell cycle related gene expression seems compensatory to the reduced cell growth. Down-regulation of the interferon-response may be explained by decreased expression of signal transducer and activator of transcription 1 upon folate deficiency. Keywords: dose response, folic acid, HT-29 cells, human
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