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RNA-seq of the human colorectal adenocarcinoma cell line HCT-116 treated with 5-aza-2’-deoxycytidine

ABSTRACT: RNA-seq of the human colorectal adenocarcinoma cell line HCT-116 treated with 5-aza-2’-deoxycytidine

PROVIDER: PRJEB56497 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR10312643_1.fastq.gz	Fastqsanger.gz
	ERR10312643_2.fastq.gz	Fastqsanger.gz
	ERR10312644_1.fastq.gz	Fastqsanger.gz
	ERR10312644_2.fastq.gz	Fastqsanger.gz
	ERR10312645_1.fastq.gz	Fastqsanger.gz

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

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RNA-seq of the human colorectal adenocarcinoma cell line HCT-116 treated with 5-aza-2’-deoxycytidine

Project description:We performed poly(A)+ stranded RNA-seq of a panel of the human colorectal adenocarcinoma cell line HCT-116 treated with 5-aza-2’-deoxycytidine. In parallel, we determined the genomic location and DNA methylation levels of human full-length LINE-1 elements (L1) from the same samples using bs-ATLAS-seq (E-MTAB-12240). To link DNA methylation and L1 expression, we used cell pellets from the same cell culture to perform both RNA-seq and bs-ATLAS-seq.

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To determine the changes in the expression of human colon cancer cells (HCT-15) untreated and treated with 5-aza-2''-deoxycytidine

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Project description:Combination therapies targeting malignancies aim to increase treatment efficacy and reduce toxicity. Hypomethylating drug 5-Aza-2’-deoxycytidine (5-Aza-2’) enhances transcription of tumor suppressor genes and induces replication errors via entrapment of DNMT1. Post-translational modification by SUMO plays major roles in the DNA damage response and is required for degradation of entrapped DNMT1. Here, we combine SUMOylation inhibitor TAK981 and DNA-hypomethylating agent 5-Aza-2’ to improve treatment of MYC driven hematopoietic malignancies, since MYC overexpressing tumors are sensitive to SUMOylation inhibition. We studied the classical MYC driven malignancy Burkitt lymphoma, as well as diffuse large B-cell lymphoma (DLBCL) with and without MYC translocation. SUMO inhibition prolonged the entrapment of DNMT1 to DNA, resulting in DNA damage. An increase in DNA damage was observed in cells co-treated with TAK981 and 5-Aza-2’. Both drugs synergized to reduce cell proliferation in vitro in a B cell lymphoma cell panel, including Burkitt lymphoma and DLBCL. In vivo experiments combining TAK981 (25 mg/kg) and 5-Aza-2’ (2.5 mg/kg) showed a significant reduction in outgrowth of Burkitt lymphoma in an orthotopic xenograft model. In contrast, single dosing of TAK981 was ineffective and single dosing of 5-Aza-2’ only led to a modest outgrowth reduction. TAK981 and 5-Aza-2’ synergize to reduce B cell Lymphoma outgrowth in vitro and in vivo. SUMOylation is a key-player in the repair of DNA damage, hence upon TAK981 treatment the repair of DNA damage induced by 5-Aza-2’ treatment is impaired. Our results demonstrate the potential of tailored combination of drugs, based on insight in molecular mechanisms, to improve the efficacy of cancer therapies.

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