| Background and Purpose:Colorectal cancer is one of the most common gastrointestinal malignancies today,with regional variations in incidence and mortality rates,but its overall trend is on the rise.Although recent developments in immunotherapy,metabolic therapy or combination therapy have led to a paradigm shift in cancer treatment and a turnaround in tumor therapy,most colorectal cancer patients have not benefited from them.Therefore,research to find new key molecules and therapeutic targets and to deeply explore the molecular mechanisms of colorectal cancer metabolism will provide a theoretical basis for comprehensive treatment strategies for colorectal cancer in clinical settings,which has important scientific research significance and clinical application prospects.In our preliminary study,we found that the key enzyme gene of glycosylation,MOGS(mannosyl-oligosaccharide glucosidase)might be a prognostic marker of colorectal cancer and correlated with the progression of tumor metastasis.Through phenotypic validation,MOGS was found to promote the proliferation and metastasis of colorectal cancer cells,which represents an important role of MOGS in the progression of colorectal carcinogenesis.It has also been shown that MOGS is involved in the invasion and metastasis of a variety of tumors,thus promoting the malignant phenotype of tumors.However,the mechanism by which MOGS regulates the malignant phenotype of tumors has not been clearly concluded,and it has not been clearly reported in colorectal cancer.The aim of this study was to investigate whether MOGS can promote the malignant phenotype of colorectal cancer and its specific regulatory mechanisms,to investigate the targeting potential of MOGS,and to provide new ideas for colorectal cancer treatment options.Methods:1、The expression of MOGS in colorectal cancer and its clinical significance were analyzed comprehensively by applying bioinformatics through public databases TCGA and GEO.2、Collect paired colorectal cancer tissue specimens and analyze the protein and mRNA expression levels of MOGS in clinical tissue specimens by RT-PCR,immunohistochemistry and Western blot techniques,and verify the statistical clinical characteristics of the bioinformatics results.3、To explore the relationship between the differential expression of MOGS in vitro level and its biological function by EDU assay and scratch assay,and to explore the influence of MOGS on the development of colorectal cancer.4、To explore the possible mechanisms of the role of MOGS in the glycosylation pathway affecting colorectal cancer,and to summarize them.Results:1.Bioinformatics results showed that MOGS was highly expressed in colorectal cancer,and the prognosis of colorectal cancer patients with high MOGS expression showed that their prognosis was worse.2.Paired clinical specimens of colorectal cancer showed that the protein and mRNA expression of MOGS was significantly higher in cancer tissues than in paracancerous tissues.3,Knockdown of MOGS expression in colorectal cancer cells in vitro inhibited the proliferation and metastasis of HCT1 16 cells.Conclusions:1,MOGS expression was significantly upregulated in colorectal cancer,and its high expression level correlated with clinical prognosis,indicating that MOGS can be used as a potential marker gene for colorectal cancer.2.MOGS was more highly expressed in clinical colorectal cancer tissues at both protein and mRNA levels than in normal tissues,which validated the raw letter results and further confirmed the potential value of MOGS as a prognostic factor in colorectal cancer.3.The phenotypic study confirmed that MOGS can promote the proliferation and migration of HCT116 cells,indicating that MOGS plays an important pro-cancer role in the development of colorectal cancer and provides a new therapeutic target for colorectal cancer. |
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