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Reuterin in the healthy gut microbiome suppresses colorectal cancer growth through altering redox balance

ABSTRACT: Reuterin in the healthy gut microbiome suppresses colorectal cancer growth through altering redox balance

PROVIDER: PRJNA776636 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR16646718_1.fastq.gz	Fastqsanger.gz
	SRR16646718_2.fastq.gz	Fastqsanger.gz
	SRR16646719_1.fastq.gz	Fastqsanger.gz
	SRR16646719_2.fastq.gz	Fastqsanger.gz
	SRR16646720_1.fastq.gz	Fastqsanger.gz

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Reuterin in the healthy gut microbiome suppresses colorectal cancer growth through altering redox balance

Project description:Microbial dysbiosis is a colorectal cancer (CRC) hallmark and contributes to inflammation, tumor growth, and therapy response. Gut microbes signal via metabolites, but how the metabolites impact CRC is largely unknown. We interrogated fecal metabolites associated with mouse models of colon tumorigenesis with varying mutational load. We found that microbial metabolites from healthy mice or humans were growth-repressive, and this response was attenuated in mice and patients with CRC. Microbial profiling revealed that Lactobacillus reuteri and its metabolite, reuterin were downregulated in mouse and human CRC. Reuterin altered redox balance, and reduced survival, and proliferation in colon cancer cells. Reuterin induced selective protein oxidation, and inhibited ribosomal biogenesis and protein translation. Exogenous Lactobacillus reuteri restricted mouse colon tumor growth, increased tumor reactive oxygen species, and decreased protein translation in vivo. Our findings indicate that a healthy microbiome and specifically, Lactobacillus reuteri, is protective against CRC through microbial metabolite exchange.

2021-12-12 | GSE186880 | GEO

Disulfiram inhbits M. tuberculosis growth by altering methionine pool and redox balance

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NTRC controls chloroplast redox homeostasis through the regulation of the redox balance of 2-Cys Prxs in Arabidopsis

Project description:Thiol-dependent redox regulation is essential for the rapid adaptation of chloroplast metabolism to unpredictable changes of light intensity. The disulfide reductase activity of thioredoxins (Trxs), which relies on photo-reduced ferredoxin (Fdx) and a Fdx-dependent Trx reductase (FTR), constitutes the Fdx-FTR-Trxs system, which links chloroplast redox regulation to light. In addition, chloroplasts harbor an NADPH-dependent Trx reductase (NTR) with a joint Trx domain, NTRC. The activity of these two redox systems is integrated by the balance of the hydrogen peroxide scavenging enzyme 2-Cys peroxiredoxin (2-Cys Prx), which thus plays a key role in maintaining the reducing capacity of chloroplast Trxs in response to light intensity. Based on the severe phenotype of mutant lines lacking NTRC, it is clear that this enzyme plays an essential role in chloroplast redox homeostasis. However, whether the function of NTRC depends on its capacity of reduce 2-Cys Prxs or has additional targets remains unknown. Here, we have addressed this issue by a comparative analysis of the triple mutant of Arabidopsis thaliana, ntrc-2cpab, simultaneously lacking 2-Cys Prxs and NTRC, and the double mutant 2cpab lacking 2-Cys Prxs. The phenotype of the ntrc-2cpab mutant is indistinguishable of the 2cpab mutant, as shown by growth rate, photosynthesis performance, light-dependent redox regulation of enzyme activity and comparative transcriptomics based RNA-Seq. Based on these results, we propose that the function of NTRC in chloroplast redox homeostasis is exerted by the regulation of the redox balance of 2-Cys Prxs rather than by the direct reduction of additional targets.

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NTRC controls chloroplast redox homeostasis through the regulation of the redox balance of 2-Cys Prxs in Arabidopsis

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Application of the redox metabolite detection method for profiling redox state following pharmacologic perturbations of redox balance in cells (part I)

Project description:This study aimed to test our optimized method for detection of redox metabolites from mammalian cells upon redox stress and metabolism perturbations. Redox balance was perturbed using H2O2 and diamide, metabolism was perturbed by methotrexate or oligomycin.

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Application of the redox metabolite detection method for profiling redox state following pharmacologic perturbations of redox balance in cells (part III)

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