Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA32167 | ENA |
REPOSITORIES: ENA
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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
2016-12-07 | GSE90403 | GEO
Project description:Expression data from HT-29 human colon adenocarcinoma cells treated with IFN-γ for 24 hr
2013-08-06 | GSE38516 | GEO
Project description:Expression data from human HT-29 immortalized colorectal adenocarcinoma cell line
| PRJNA140239 | ENA
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.
2013-08-06 | E-GEOD-38516 | biostudies-arrayexpress
Project description:Colorectal cancer HT-29 cell line is a comonly-used human cancer cell line. We have used this cell line for examining the effect of various anticancer compounds on gene expression and we obtained gene expression data of untreated HT-29 cells as a control data for the analysis.
2017-06-14 | GSE99968 | GEO
Project description:CDK8 knockdown in HT-29 human colon cancer cells
| PRJNA154569 | ENA
Project description:First, in a model of xenografts induced with HT-29 human colon cancer cells, we demonstrated that the transcription factor NF-kB was involved in the resistance to CPT-11. Then, from one tumor treated with CPT-11 plus a NF-kB inhibitor, we established a resistant cell line to CPT-11. The aim of this study was to compare the expression of genes involved in the signaling pathway of NF-kB between the sensitive and the resistant cell lines and to identify other genes (target or not of NF-kB) which the expression was modified when the resistant phenotype was acquired. Human colon cancer cells chemosensitive (HT-29) versus human colon cancer cells chemoresistant (RIV) in a dye-swap experiment.
2012-08-23 | E-GEOD-23433 | biostudies-arrayexpress
Project description:Metastasis and drug-resistance are major problems in cancer chemotherapy. The purpose of this work was to analyze the molecular mechanisms underlying the invasive potential of drug-resistant colon carcinoma cells. Cellular models included the parental HT-29 cell line and its drug-resistant derivatives selected after chronic treatment with either 5-fluorouracil (5-FU), methotrexate (MTX), doxorubicin (DOX) or oxaliplatin (OXA). Drug-resistant invasive cells were compared to non invasive cells using cDNA microarray, qRT-PCR, flow cytometry, immunoblots and ELISA. Functional and cellular signaling analyses were undertaken using pharmacological inhibitors, function-blocking antibodies, and silencing by retrovirus-mediated RNA interference. 5-FU- and MTX-resistant HT-29 cells expressing an invasive phenotype in collagen type I and a metastatic behaviour in immunodeficient mice exhibited high expression of the chemokine receptor CXCR4. Macrophage migration inhibitory factor (MIF) was identified as the critical autocrine CXCR4 ligand promoting invasion in drug-resistant colon carcinoma HT-29 cells. Silencing of CXCR4 and impairing the MIF-CXCR4 signaling pathways by ISO-1, pAb FL-115, AMD-3100, mAb 12G5, and BIM-46187 abolished this aggressive phenotype. Induction of CXCR4 is associated with up-regulation of two genes encoding transcription factors previously shown to control CXCR4 expression (HIF-2a and ASCL2) and maintenance of intestinal stem cells (ASCL2). Enhanced CXCR4 expression was detected in liver metastases resected from colon cancer patients treated by the standard FOLFOX regimen. Combination therapies targeting the CXCR4-MIF axis can potentially counteract the emergence of the invasive metastatic behaviour in clonal derivatives of drug-resistant colon cancer cells. Samples: HT-29 cell clones were obtained by limiting dilution from HT-29 subpopulations resistant to methothrexate (HT-29 5M21 cell clone) and or to 5-Fluoro-uracil (HT-29 5F7 and HT-29 5F31). Samples were provided by Dr. T Lesuffleur. Xenografts: HT-29 5M21, HT-29 5F7, and HT-29 5F31 xenografts were obtained by a first subcutaneous inoculation of cells in Nude mice and then fragments of subcutaneous tumors were reimplantated in SCID mice. First experiment of microarrays: HT-29 5M21 and HT-29 5F7 cells (that are invasive in in vitro assays on type I collagen) were compared to HT-29 5F31 cells (that are not invasive in vitro on type I collagen). Samples were co-hybridized on Agilent Human 44K GEP arrays (respectively 5F31 vs 5M21, 5F31 vs 5F7, 5M21 vs 5F31 and 5F7 vs 5F31). Second experiment of microarrays: HT-29 5M21 and HT-29 5F7 xenografts (that develop metastases in immuno-deficient mice lungs) were compared to HT-29 5F31 xenografts (that do not develop metastases in immuno-deficient mice lungs). Samples were consequently co-hybridized on human and mouse 4x44K GEP arrays (respectively AG41_5F31-5M21-138869, AG39_5F31-5F7-138867, AG42_5M21-5F31-138870 and AG40_5F7-5F31-138868 for human microarrays; 5M21_5F31_27033_4, 5F31_5M21_27033_3, 5F7_5F31_27033_2 and 5F31_5F7_27033_1_1 for mouse microarrays).
2010-07-07 | E-GEOD-20147 | biostudies-arrayexpress
Project description:Expression data from HT-29, a human colonic epithelial cell line
| PRJNA193228 | ENA
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