Effective oxygen metabolism-based prognostic signature for colorectal cancer

BackgroudOxygen metabolism is an important factor affecting the development of tumors, but its roles and clinical value in Colorectal cancer are not clear. We developed an oxygen metabolism (OM) based prognostic risk model for colorectal cancer and explored the role of OM genes in cancer. MethodsGene expression and clinical data obtained from The Cancer Genome Atlas, Clinical Proteomic Tumor Analysis Consortium databases were consider as discovery and validation cohort, respectively. The prognostic model based on differently expressed OM genes between tumor and GTEx normal colorectal tissues were constructed in discovery cohort and validated in validation cohort. The Cox proportional hazards analysis was used to test clinical independent. Upstream and downstream regulatory relationships and interaction molecules are used to clarify the roles of prognostic OM genes in colorectal cancer. ResultsA total of 72 common differently expressed OM genes were detected in the discovery and validation set. A five-OM gene prognostic model including LRT2, ATP6V0E2, ODC1, SEL1L3 and VDR was established and validated. Risk score determined by the model was an independent prognostic according to routine clinical factors. Besides, the role of prognostic OM genes involves transcriptional regulation of MYC and STAT3, and downstream cell stress and inflammatory response pathways. ConclusionsWe developed a five-OM gene prognostic model and study the unique roles of oxygen metabolism in of colorectal cancer

Automated summary

We developed an oxygen metabolism-based prognostic risk model for colorectal cancer and investigated the role of oxygen metabolism genes in cancer. A five-gene prognostic model including LRT2, ATP6V0E2, ODC1, SEL1L3, and VDR was established and validated. The risk score determined by the model was an independent prognostic indicator, and the prognostic genes were involved in the transcriptional regulation of MYC and STAT3, as well as downstream cell stress and inflammatory response pathways in colorectal cancer.