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Genome-wide binding signature of Signal transducer and activator of transcription (STAT) family in colorectal cancer HCT 116 cell

ABSTRACT: Genome-wide binding signature of Signal transducer and activator of transcription (STAT) family in colorectal cancer HCT 116 cell

PROVIDER: PRJEB48487 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR7198360_1.fastq.gz	Fastqsanger.gz
	ERR7198360_2.fastq.gz	Fastqsanger.gz
	ERR7198370_1.fastq.gz	Fastqsanger.gz
	ERR7198370_2.fastq.gz	Fastqsanger.gz
	ERR7198361_1.fastq.gz	Fastqsanger.gz

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Genome-wide binding signature of Signal transducer and activator of transcription (STAT) family in colorectal cancer HCT 116 cell

Project description:The excessive and continuous activated Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway leads to the proliferation and migration of malignant cells resulting in the occurrence and development of almost all of cancers. The defined gene sets specifically activated by different STAT proteins are relied on their genomic accessibility by the interplay of certain STAT proteins with other potential cofactors. However, we have no clue about the status of human activated STAT dimers in the nucleus, as well as the intercrossing modules of synergic, supplementary or competitive relationship among each other in colorectal cancer. In current study, chromatin immunoprecipitation sequencing (ChIP-seq) was conducted to explore the genome-scale binding signatures of STAT1, STAT2, STAT3, STAT5A/B and STAT6 in human HCT-116 CRC cells. Moreover, STAT3 binding on genomic DNA was also investigated in HCT116 cells with NR5A2 knockdown.

2021-11-08 | E-MTAB-11113 | biostudies-arrayexpress

MicroRNA profiling of HCT-116 versus HCT-116 treated with 5-aza-2'-deoxycytidine processing human colon cancer cell lines

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Expression data in HCT-116 colon cancer cell treated with SCD1 inhibitor or in SCD1 knocked out HCT-116 cell

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Project description:Anti-APC ChIP-seq data were collected from HCT-116 cells and 3,985 genomic sequences were found to be enriched in both independent biological replicates.

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Gene expression profile of human colorectal carcinoma HCT 116 cell line treated with imipramine

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Gene alterations by PPAR-gamma agonists in human colorectal adenocarcinoma HCT-116 cells

Project description:We examined the alternation of gene expression by MCC-555, rosiglitazone (RGZ) and 15-deoxy-Δ12, 14-prostaglandin J2 (PGJ2) in human colorectal adenocarcinoma HCT-116 cells. Keywords: effects of PPAR-gamma agonists

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Homo sapiens strain:HCT-116 cell lines

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Barcode and Whole Exome Sequencing Data of Dabrafenib Resistant 3D-HT-29 and Irinotecan Resistant 3D-HCT-116 Spheroids

Project description:HT-29 and HCT-116 cells were barcoded using the CloneTracker lentiviral barcode library and then dabrafenib and irinotecan resistant derivatives of these cell lines were established, respectively.10 million barcoded HT-29 and HCT-116 cells were seeded equally onto poly-HEMA coated 4xT75 flask (DMSO Control, Replica A, B, C for each drug). After seeding, cells were allowed to form spheroids and barcoded 3D-HT-29 spheroids were treated with dabrafenib at increasing doses starting from IC50/10 dose until IC50/2 dose with monthly doubling of the dosing (16 weeks), and barcoded 3D-HCT-116 cells were treated with irinotecan at increasing doses starting from IC50/4 dose until IC50 dose with weekly doubling of the dosing (4 weeks). Following the end points of treatment for each cell line, DNA was isolated from harvested cell lines and barcode sequencing and whole exome sequencing were carried out.

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