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Epigenetic profiling of H3K4me3 reveals Herbal Medicine Jinfukang-induced epigenetic alteration is involved in anti-Lung Cancer activity

ABSTRACT: Epigenetic profiling of H3K4me3 reveals Herbal Medicine Jinfukang-induced epigenetic alteration is involved in anti-Lung Cancer activity

PROVIDER: PRJEB11756 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1125541.fastq.gz	Fastqsanger.gz
	ERR1125542.fastq.gz	Fastqsanger.gz
	ERR1125543.fastq.gz	Fastqsanger.gz
	ERR1125544.fastq.gz	Fastqsanger.gz

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Epigenetic profiling of H3K4me3 reveals Herbal Medicine Jinfukang-induced epigenetic alteration is involved in anti-Lung Cancer activity

Project description:Traditional Chinese medicine Jinfukang (JFK) has been used for lung cancer treatment for more than ten years, however, the mechanism is not well understood. Previously we showed that JFK inhibited survival of a human lung cell line A459 via cell apoptosis and inducing cell cycle arrest. To better understand the mechanism, we performed ChIP-seq assays to evaluate the effect of JFK on genome-wide profiling of H3K4Me3 modification.

2016-06-01 | E-MTAB-3992 | biostudies-arrayexpress

Epigenetic Profiling of H3K4Me3 Reveals Herbal Medicine Jinfukang-Induced Epigenetic Alteration Is Involved in Anti-Lung Cancer Activity.

Project description:Traditional Chinese medicine Jinfukang (JFK) has been clinically used for treating lung cancer. To examine whether epigenetic modifications are involved in its anticancer activity, we performed a global profiling analysis of H3K4Me3, an epigenomic marker associated with active gene expression, in JFK-treated lung cancer cells. We identified 11,670 genes with significantly altered status of H3K4Me3 modification following JFK treatment (P < 0.05). Gene Ontology analysis indicates that these genes are involved in tumor-related pathways, including pathway in cancer, basal cell carcinoma, apoptosis, induction of programmed cell death, regulation of transcription (DNA-templated), intracellular signal transduction, and regulation of peptidase activity. In particular, we found that the levels of H3K4Me3 at the promoters of SUSD2, CCND2, BCL2A1, and TMEM158 are significantly altered in A549, NCI-H1975, NCI-H1650, and NCI-H2228 cells, when treated with JFK. Collectively, these findings provide the first evidence that the anticancer activity of JFK involves modulation of histone modification at many cancer-related gene loci.

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