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Dietary tyramine promotes colon cancer risk and development via increased DNA damage and enhanced Inflammation

ABSTRACT: Dietary tyramine promotes colon cancer risk and development via increased DNA damage and enhanced Inflammation

PROVIDER: PRJNA985629 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24792000_1.fastq.gz	Fastqsanger.gz
	SRR24792000_2.fastq.gz	Fastqsanger.gz
	SRR24792001_1.fastq.gz	Fastqsanger.gz
	SRR24792001_2.fastq.gz	Fastqsanger.gz
	SRR24792002_1.fastq.gz	Fastqsanger.gz

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Dietary tyramine promotes colon cancer risk and development via increased DNA damage and enhanced Inflammation [HCT116]

Project description:High dietary consumption of red or processed meat is associated with increased risk of colorectal cancer (CRC), likely through the presence of dietary carcinogens. Tyramine is a biogenic amine commonly found in processed food and can be produced by the gut bacteria from tyrosine. However, the role of tyramine in intestinal mucosal health has not been studied. Therefore, we used the human colonic HCT116 cell line to investigate the role of tyramine in modulating CRC risk and development

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Dietary tyramine promotes colon cancer risk and development via increased DNA damage and enhanced inflammation [ApcMin/+]

Project description:High consumption of dietary red or processed meat and fat are linked to increased risk of colorectal cancer (CRC). A number of potential mechanisms have been reported, such as the presence of dietary carcinogenic compounds, and elevated gut microbial degradation of proteins and glycoproteins. Tyramine is a commonly found biogenic amine in processed food and can also be produced by the gut microbiota from the dietary amino acid tyrosine. The role of tyramine in intestinal mucosal health and CRC tumorigenesis has not been well studied. Therefore, we used the human colorectal HCT116 cell line and the ApcMin/+ mouse model to investigate the role of tyramine in CRC.

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Dietary tyramine promotes colon cancer risk and development via increased DNA damage and enhanced Inflammation

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Enterococcus-derived tyramine hijacks α2A-adrenergic receptor in intestinal stem cells to exacerbate colitis

Project description:Inflammatory bowel disease (IBD) is characterized by dysbiosis of the gut microbiota and dysfunction of in testinal stem cells (ISCs). However, the direct interactions between IBD microbial factors and ISCs are unde scribed. Here, we identify α2A-adrenergic receptor (ADRA2A) as a highly expressed GPCR in ISCs. Through PRESTO-Tango screening, we demonstrate that tyramine, primarily produced by Enterococcus via tyrosine decarboxylase (tyrDC), serves as a microbial ligand for ADRA2A. Using an engineered tyrDC deficient Enterococcus faecalis strain and intestinal epithelial cell-specific Adra2a knockout mice, we show that Enterococcus-derived tyramine suppresses ISC proliferation, thereby impairing epithelial regeneration and exacerbating DSS-induced colitis through ADRA2A. Importantly, blocking the axis with an ADRA2A antagonist, yohimbine, disrupts tyramine-mediated suppression on ISCs and alleviates colitis.Our findings highlight a microbial ligand-GPCR pair in ISCs, revealing a causal link between microbial regulation of ISCs and colitis exacerbation and yielding a targeted therapeutic approach to restore ISC function in colitis.

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