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ABSTRACT: Roseburia intestinalis sensitizes colorectal cancer to radiotherapy through butyrate/OR51E1/RALB axis

PROVIDER: PRJNA1067426 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27675810.fastq.gz	Fastqsanger.gz
	SRR27675811.fastq.gz	Fastqsanger.gz
	SRR27675812.fastq.gz	Fastqsanger.gz
	SRR27675813.fastq.gz	Fastqsanger.gz
	SRR27675814.fastq.gz	Fastqsanger.gz

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Radiotherapy for CRC (FMT)

Project description:Roseburia sensitizes colorectal cancer to radiotherapy

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The Human Gut Firmicute Roseburia intestinalis is a Primary Degrader of Dietary β-Mannans

Project description:β-Mannans are plant cell wall polysaccharides that are commonly found in human diets. However, a mechanistic understanding into the key populations that degrade this glycan is absent, especially for the dominant Firmicutes phylum. Here, we show that the prominent butyrate-producing Firmicute Roseburia intestinalis expresses two loci conferring metabolism of β-mannans. We combine multi-“omic” analyses and detailed biochemical studies to comprehensively characterize loci-encoded proteins that are involved in β-mannan capturing, importation, de-branching and degradation into monosaccharides. In mixed cultures, R. intestinalis shares the available β-mannan with Bacteroides ovatus, demonstrating that the apparatus allows coexistence in a competitive environment. In murine experiments, β-mannan selectively promotes beneficial gut bacteria, exemplified by increased R. intestinalis, and reduction of mucus-degraders. Our findings highlight that R. intestinalis is a primary degrader of this dietary fiber and that this metabolic capacity could be exploited to selectively promote key members of the healthy microbiota using β-mannan-based therapeutic interventions.

2019-02-21 | PXD012448 | Pride

Interactions between Roseburia intestinalis and diet modulate atherogenesis in a murine model

Project description:Background: Humans with metabolic and inflammatory diseases frequently harbor lower levels of butyrate-producing bacteria in their gut. However, it is not known whether variation in the levels of these organisms is causally linked with disease development and whether diet modifies the impact of these bacteria on health. Results: We use germ-free apolipoprotein E-deficient mice colonized with synthetic microbial communities that differ in their capacity to generate butyrate to demonstrate that Roseburia intestinalis interacts with dietary components to (i) impact gene expression in the intestine, directing metabolism away from glycolysis and toward fatty acid utilization, (ii) improve intestinal barrier function, (iii) lower systemic inflammation and (iv) ameliorate atherosclerosis. Furthermore, intestinal administration of butyrate improves gut barrier function and reduces atherosclerosis development. Conclusions: Altogether, our results illustrate how modifiable diet-by-microbiota interactions impact cardiovascular disease, and suggest that interventions aimed at increasing the representation of butyrate-producing bacteria may provide protection against atherosclerosis.

2018-08-29 | GSE119141 | GEO

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Project description:Roseburia intestinalis overview

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Roseburia intestinalis CAG:13

Project description:Roseburia intestinalis CAG:13 overview

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Project description:Xylan utilization by Roseburia intestinalis

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Sodium butyrate-induced autophagy in colorectal cancer unveils the Ca²⁺/CaMKKβ signaling pathway as a potential therapeutic target

Project description:Sodium butyrate and colorectal cancer

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Project description:β-Mannan utilization by Roseburia intestinalis

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Roseburia intestinalis XB6B4

Project description:Roseburia intestinalis XB6B4 genome sequencing project

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CNOT7 Promotes Radiation Resistance in Colorectal Cancer via XRCC6-Mediated NHEJ DNA Repair Pathway

Project description:In this study, we identified CNOT7 as a key protein influencing the radiotherapy sensitivity of rectal cancer through proteomic sequencing of patient tissues. Patients with high CNOT7 expression often exhibit poorer prognoses during radiotherapy. We explored the potential mechanisms by which CNOT7 affects radiotherapy sensitivity in CRC. CNOT7 reduces polyubiquitination of K48 linked lysine 526 on XRCC6 by regulating TRIM21. This enhances DNA damage repair primarily mediated by the NHEJ pathway, thereby conferring radiotherapy resistance to colorectal cancer cells. Our study suggests that targeting CNOT7 could serve as a potential therapeutic strategy for rectal cancer patients

2025-04-28 | GSE287014 | GEO

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