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Effect of folic acid deprivation on H3K27me3 and H3K9me2 upon OTX treatment

ABSTRACT: Effect of folic acid deprivation on H3K27me3 and H3K9me2 upon OTX treatment

PROVIDER: PRJNA639368 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12010532.fastq.gz	Fastqsanger.gz
	SRR12010533.fastq.gz	Fastqsanger.gz
	SRR12010534.fastq.gz	Fastqsanger.gz
	SRR12010535.fastq.gz	Fastqsanger.gz
	SRR12010536.fastq.gz	Fastqsanger.gz

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Effect of folic acid deprivation on on transcriptome upon OTX treatment

Project description:Effect of folic acid deprivation on on transcriptome upon OTX treatment

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A folic acid-enriched diet attenuates prostate involution in response to androgen deprivation

Project description:Folic acid is present in pre-natal vitamins, fortified cereal grains and multi-vitamin supplements. High intake of folic acid through these sources has resulted in populations with increased levels of serum folate and unmetabolized folic acid. Although the benefits of folic acid in the prevention of neural tube defects are undeniable, the impact of long-term consumption of folic acid on the prostate is not fully understood. In this study, we used a rodent model to test whether dietary folic acid (FA) supplementation changes prostate homeostasis and response to androgen deprivation. Although intact prostate weights do not differ between diet groups, we made the surprising observation that dietary folic acid supplementation confers partial resistance to castration-mediated prostate involution. More specifically, male mice that were fed a folic acid supplemented diet and then castrated had greater prostate wet weights, greater prostatic luminal epithelial cell heights, and more abundant RNAs encoding prostate secretory proteins compared to mice that were fed a control diet and castrated. We used RNA-seq to identify signaling pathways enriched in the castrated prostates from folic acid supplemented diet fed mice compared to control mice. We observed differential expression of genes involved in several metabolic pathways in the FA supplemented mice. Together, our results show that dietary FA supplementation can impact metabolism in the prostate and attenuate the prostate’s response to androgen deprivation. This has important implications for androgen deprivation therapies used in the treatment of prostate disease, as consumption of high levels of folic acid could reduce the efficacy of these treatments.

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Effect of folic acid deprivation on H3K27me3 and H3K9me2 upon OTX treatment

Project description:Deciphering the impact of metabolic intervention on response to anticancer therapy represents a path toward improved clinical responses. Here, we identify amino acid-related pathways connected to the folate cycle whose activation predicts sensitivity to MYC-targeting therapies in acute myeloid leukemia (AML). We establish that folate restriction and deficiency of the rate-limiting folate-cycle enzyme, MTHFR ― which exhibits reduced-function polymorphisms in about 10% of Caucasians ― enhance resistance to MYC targeting by BET and CDK7 inhibitors in cell lines, primary patient samples and syngeneic mouse models of AML. Further, this effect is abrogated by supplementation with the MTHFR enzymatic product, CH3-THF. Mechanistically, folate cycle disturbance reduces H3K27/K9 histone methylation, and activates a SPI1 transcriptional program counteracting the effect of BET inhibition. Our data provide a rationale for screening MTHFR polymorphisms and the folate cycle status to exclude patients least likely and nominate those most likely to benefit from MYC-targeting therapies.

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The genomic distribution of G9a, H3K9me2 and H3K27me3 in cardiac hypertrophy.

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ChIP-chip of H3K4Me1, H3K4Me3, H3K4Ac, H3K9Ac, H3K9Me2, H3K27Me3, CTCF and HP1a in MCF7 breast cancer cells

Project description:We report the high-throughput profiling of histone modifications, CTCF and HP1a binding sites in MCF7 breast cancer cells. ChIP-chip experiments were performed using the Agilent Human Genome CGH Microarray 1x1M. Regulatory markers H3K4Me1, H3K4Me3, H3K4Ac, H3K9Ac, CTCF are known to be positively correlated with gene expression, and H3K9Me2, H3K27Me3 and HP1a are negative markers. Together with MCF7 methylation data, we showed hypomethylated promoters are significantly enriched with positive regulatory elements, and lacks repressive markers.

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