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2016 ; 4
(ä): 11
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Metabolomics and metabolic pathway networks from human colorectal cancers,
adjacent mucosa, and stool
#MMPMID27275383
Brown DG
; Rao S
; Weir TL
; O'Malia J
; Bazan M
; Brown RJ
; Ryan EP
Cancer Metab
2016[]; 4
(ä): 11
PMID27275383
show ga
BACKGROUND: Colorectal cancers (CRC) are associated with perturbations in
cellular amino acids, nucleotides, pentose-phosphate pathway carbohydrates, and
glycolytic, gluconeogenic, and tricarboxylic acid intermediates. A non-targeted
global metabolome approach was utilized for exploring human CRC, adjacent mucosa,
and stool. In this pilot study, we identified metabolite profile differences
between CRC and adjacent mucosa from patients undergoing colonic resection.
Metabolic pathway analyses further revealed relationships between complex
networks of metabolites. METHODS: Seventeen CRC patients participated in this
pilot study and provided CRC, adjacent mucosa ~10 cm proximal to the tumor, and
stool. Metabolomes were analyzed by gas chromatography-mass spectrometry (GC/MS)
and ultra-performance liquid chromatography-mass spectrometry (UPLC-MS/MS). All
of the library standard identifications were confirmed and further analyzed via
MetaboLync(TM) for metabolic network interactions. RESULTS: There were a total of
728 distinct metabolites identified from colonic tissue and stool matrices.
Nineteen metabolites significantly distinguished CRC from adjacent mucosa in our
patient-matched cohort. Glucose-6-phosphate and fructose-6-phosphate demonstrated
0.64-fold and 0.75-fold lower expression in CRC compared to mucosa, respectively,
whereas isobar: betaine aldehyde, N-methyldiethanolamine, and adenylosuccinate
had 2.68-fold and 1.88-fold higher relative abundance in CRC. Eleven of the 19
metabolites had not previously been reported for CRC relevance. Metabolic pathway
analysis revealed significant perturbations of short-chain fatty acid metabolism,
fructose, mannose, and galactose metabolism, and glycolytic, gluconeogenic, and
pyruvate metabolism. In comparison to the 500 stool metabolites identified from
human CRC patients, only 215 of those stool metabolites were also detected in
tissue. This CRC and stool metabolome investigation identified novel metabolites
that may serve as key small molecules in CRC pathogenesis, confirmed the results
from previously reported CRC metabolome studies, and showed networks for
metabolic pathway aberrations. In addition, we found differences between the CRC
and stool metabolomes. CONCLUSIONS: Stool metabolite profiles were limited for
direct associations with CRC and adjacent mucosa, yet metabolic pathways were
conserved across both matrices. Larger patient-matched CRC, adjacent
non-cancerous colonic mucosa, and stool cohort studies for metabolite profiling
are needed to validate these small molecule differences and metabolic pathway
aberrations for clinical application to CRC control, treatment, and prevention.