International Journal of Cancer · 2018 · 115 citations · 47 references
Life SciencesBiochemistryCancer BiologyMetabolismMetabolomicsMicrobiome ResearchCancer MetabolomicsGut MicrobiomeGut MicrobiotaMetabolite IdentificationMetabolite ProfilingMicrobial Community ProfilingGut Microbiota CompositionLiquid Chromatography-mass SpectrometryLiquid Chromatography-mass Spectrometry AnalysisMetabolomic ChangesMicrobial Community MetabolomicsMicrobial Community StructureMicrobiome-associated MetabolitesMicrobiota Biomarkers
The aim of our study was to investigate the relationship among the gut microbiota community, metabolite profiles and thyroid carcinoma (TC). First, 30 TC patients and 35 healthy controls (HCs) fecal samples were applied to characterize the gut microbial community using 16S rRNA gene sequencing. Differential microbiota compositions were observed, with significant enrichment of 19 and depletion of 8 genera in TC samples compared to those in HCs (Q value <0.05), and some genera were correlated with various clinical parameters, such as lipoprotein A and apolipoprotein B. Furthermore, 6 different genera distinguished TC patients from HCs with the AUC of 0.94. The PICRUSt analysis showed 12 remarkably different metabolic pathways (Q value <0.05). Subsequently, we systematically analyzed the gut microbiota and metabolites in the same TC patients (n = 15) and HCs (n = 15). The characteristics of the gut microbiota community were mostly consistent with the above results (30 TC patients and 35 HCs), and liquid chromatography mass spectrometry analysis was performed to characterize the metabolite profiles. In total, 21 different genera (Q value <0.05) and 72 significantly changed metabolites (VIP > 1.0 and p < 0.05) were observed and correlated to each other. Eight metabolites combined with 5 genera were more effective in distinguishing TC patients from HCs (AUC = 0.97). In conclusion, our study presents a comprehensive landscape of the gut microbiota and metabolites in TC patients, and provides a research direction of the mechanism of interaction between gut microbiota alteration and TC pathogenesis.
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