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DNA methylation analysis of colorectal cancer SW48/YB5 cell line treated with the HH1 compound

ABSTRACT: DNA methylation analysis of colorectal cancer SW48/YB5 cell line treated with the HH1 compound

PROVIDER: PRJNA414395 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6175600.fastq.gz	Fastqsanger.gz
	SRR6175610.fastq.gz	Fastqsanger.gz
	SRR6175601.fastq.gz	Fastqsanger.gz
	SRR6175602.fastq.gz	Fastqsanger.gz
	SRR6175603.fastq.gz	Fastqsanger.gz

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DNA methylation analysis of colorectal cancer SW48/YB5 cell line treated with the HH1 compound

Project description:YB5 is a colon cancer cell line derived from the SW48 colon cancer cell line and contains a DNA methylated and silenced CMV promoter driving expression of a GFP reporter. The cells were treated with 10 micromolar concentration of the HH1 compound or with DMSO as a control. Reduced representation bisulfite sequencing (RRBS) was performed after the treatment to analyze DNA methylation at CpG sites.

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RNA-seq of YB5 cells treated with HH1

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Effect of decitabine, carboplatin and their combination on gene expression in the YB5 colon cancer cell line.

Project description:YB5 cell line is a clonal derivative of the SW48 colon cancer cell line that contains a single copy of a green fluorescent protein (GFP) reporter silenced by CpG methylation at its CMV promoter. We treated the YB5 cells with decitabine (5-aza-2’-deoxycytidine), carboplatin and the combination of decitabine plus carboplatin and analyzed the effects of the drugs on gene expression.

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RNA-seq of YB5 cells treated with HH1

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Gene expression of colorectal cancer cells treated with Celastrol or compound 19-048

Project description:As a terpenoids natural product isolated from the plant Thunder God Vine, Celastrol is widely studied for its pharmacological activities, including anti-tumor activities. However, the clinical application of Celastrol is strictly limited due to its severe side effects. Without identification and validation of the target protein of Celastrol, it is difficult to determine whether its anti-tumor activities and side effects are due to inhibition of the same protein. Using a new computational tool we have developed for target discovery, peroxiredoxin I (PRDX1) was identified as the ROS-manipulating target protein of Celastrol. High-resolution crystal structure revealed the unique binding mode of Celastrol with PRDX1, via covalent reaction to the catalytic Cys-173 residue of PRDX1. New derivative compound named 19-048 with improved potency against PRDX1 and selectivity towards PRDX2~PRDX6 were synthesized. Both Celastrol and compound 19-048 effectively suppressed the proliferation of colorectal cancer cells. While these anti-tumor efficacy was significantly diminished on xenograft nude mice bearing PRDX1 knock-down colorectal cancer cells. Several downstream genes of p53 were dramatically up-regulated in the presence of Celastrol and compound 19-048. Our findings reveal that the side effects of Celastrol could be reduced via structural modification, and PRDX1 inhibition is promising for the treatment of colorectal cancer.

2022-12-31 | GSE198630 | GEO

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