Multi-omics analyses of glucose metabolic reprogramming in colorectal cancer

Background Glucose metabolic reprogramming (GMR) is a cardinal feature of carcinogenesis and metastasis. However, the underlying mechanisms have not been fully elucidated. The aim this study was to profile signature primary tumor circulating cells from metastatic colorectal cancer (mCRC) patients using integrated omics analysis. Methods PET-CT imaging, serum metabolomics, genomics proteomics data 325 high 18F-fluorinated deoxyglucose (FDGhigh) mCRC were analyzed. para-tumor, liver tissues used for Results glucose uptake in as per PET/CT images correlated levels glutamic-pyruvic transaminase (ALT), total bilirubin (TBIL), creatinine (CRE). Proteomics analysis indicated that several differentially expressed proteins enriched both GMR epithelial-mesenchymal transition (EMT)-related pathways. Using tissue-optimized proteomic workflow, we identified novel markers (e.g. CCND1, EPCAM, RPS6), PCK1-CDK6-INSR protein axis, potential role FOLR (FR) GMR/EMT CRC cells. Finally, CEA/blood (CSR) defined new index, which can be jointly diagnose metastasis cancer. Conclusions closely associated with EMT pathway, network promising source therapeutic targets.