Project description:Increasing evidence indicates that gut microbiota plays an important role in cancer progression. We have employed RNA-seq or microarray for genome including mRNA, microRNA or circRNA profiling in an gut microbiota -dependent manner, as a discovery platform to identify target genes with the potential to involve in tumor regulation. The deep sequencing analysis reveals regulatory functions of microbiota-mediated circular RNA (circRNA)/microRNA networks that may contribute to cancer progression.
Project description:Increasing evidence indicates that gut microbiota plays an important role in cancer progression. We have employed RNA-seq or microarray for genome including mRNA, microRNA or circRNA profiling in an gut microbiota -dependent manner, as a discovery platform to identify target genes with the potential to involve in tumor regulation. The deep sequencing analysis reveals regulatory functions of microbiota-mediated circular RNA (circRNA)/microRNA networks that may contribute to cancer progression.
Project description:Increasing evidence indicates that gut microbiota plays an important role in cancer progression. We have employed RNA-seq or microarray for genome including mRNA, microRNA or circRNA profiling in an gut microbiota -dependent manner, as a discovery platform to identify target genes with the potential to involve in tumor regulation. The deep sequencing analysis reveals regulatory functions of microbiota-mediated circular RNA (circRNA)/microRNA networks that may contribute to cancer progression.
Project description:Increasing evidence indicates that gut microbiota plays an important role in cancer progression. We have employed RNA-seq or microarray for genome including mRNA, microRNA or circRNA profiling in an gut microbiota -dependent manner, as a discovery platform to identify target genes with the potential to involve in tumor regulation. The deep sequencing analysis reveals regulatory functions of microbiota-mediated circular RNA (circRNA)/microRNA networks that may contribute to cancer progression.
Project description:Gut microbiota dysbiosis characterizes systemic metabolic alteration, yet its causality is debated. To address this issue, we transplanted antibiotic-free conventional wild-type mice with either dysbiotic (“obese”) or eubiotic (“lean”) gut microbiota and fed them either a NC or a 72%HFD. We report that, on NC, obese gut microbiota transplantation reduces hepatic gluconeogenesis with decreased hepatic PEPCK activity, compared to non-transplanted mice. Of note, this phenotype is blunted in conventional NOD2KO mice. By contrast, lean microbiota transplantation did not affect hepatic gluconeogenesis. In addition, obese microbiota transplantation changed both gut microbiota and microbiome of recipient mice. Interestingly, hepatic gluconeogenesis, PEPCK and G6Pase activity were reduced even once mice transplanted with the obese gut microbiota were fed a 72%HFD, together with reduced fed glycaemia and adiposity compared to non-transplanted mice. Notably, changes in gut microbiota and microbiome induced by the transplantation were still detectable on 72%HFD. Finally, we report that obese gut microbiota transplantation may impact on hepatic metabolism and even prevent HFD-increased hepatic gluconeogenesis. Our findings may provide a new vision of gut microbiota dysbiosis, useful for a better understanding of the aetiology of metabolic diseases. all livers are from NC-fed mice only.
Project description:To compare the similarities and differences in species diversity of the gut microbiota between the patients with melasma and healthy subjects. The feces were collected for 16S rRNA sequencing analysis of the gut microbiota.
Project description:In the presented study, in order to unravel gut microbial community multiplicity and the influence of maternal milk nutrients (i.e., IgA) on gut mucosal microbiota onset and shaping, a mouse GM (MGM) was used as newborn study model to discuss genetic background and feeding modulation on gut microbiota in term of symbiosis, dysbiosis and rebiosis maintenance during early gut microbiota onset and programming after birth. Particularly, a bottom-up shotgun metaproteomic approach, combined with a computational pipeline, has been compred with a culturomics analysis of mouse gut microbiota, obtained by MALDI-TOF mass spectrometry (MS).
Project description:Gut microbial profiling of uterine fibroids (UFs) patients comparing control subjects. The gut microbiota was examined by 16S rRNA quantitative arrays and bioinformatics analysis. The goal was to reveal alterations in the gut microbiome of uterine fibroids patients.
Project description:Gut microbiota and their metabolites influence host gene expression and physiological status through diverse mechanisms. Here we investigate how gut microbiota and their metabolites impact host's mRNA m6A epitranscriptome in various antibiotic-induced microbiota dysbiosis models. With multi-omics analysis, we find that the imbalance of gut microbiota can rewire host mRNA m6A epitranscriptomic profiles in brain, liver and intestine. We further explore the underlying mechanisms regulating host mRNA m6A methylome by depleting the microbiota with ampicillin. Metabolomic profiling shows that cholic acids are the main down-regulated metabolites with Firmicutes as the most significantly reduced genus in ampicillin-treated mice comparing to untreated mice. Fecal microbiota transplantations in germ-free mice and metabolites supplementations in cells verify that cholic acids are associated with host mRNA m6A epitranscriptomic rewiring. Collectively, this study employs an integrative multi-omics analysis to demonstrate the impact of gut microbiota dysbiosis on host mRNA m6A epitranscriptomic landscape via cholic acid metabolism.