ObjectiveThrough the analysis of gene enrichment in gastric cancer samples, the changes of RNA alternative splicing and related molecular mechanisms were explored.MethodsThe pathological samples of three cases of gastric cancer patients and adjacent tissues were obtained clinically, and the data were obtained by cell culture, protein quantitative labeling, gene chip detection, high-throughput sequencing, etc. GO enrichment was performed on samples by DAVID and other network software, KEGG pathway analysis yielded relevant information for screening for variable splicing of differential genes.ResultsA total of 605 genes with individual ENSG IDs consistent with the gene identification of the ENSEMBL database were screened, and the gene levels of cancer tissues and adjacent tissues were compared. There were 411 non-differentiated genes, 119 differentially up-regulated genes, and 75 differentially down-regulated genes. A total of 69 differentially spliced genes were screened out. Functional annotation and pathway analysis revealed that the detection genes were mainly concentrated in molecular metabolic processes, cell migration, extracellular matrix tissue, blood coagulation, cell matrix adhesion, signal transduction, negative apoptosis regulation, angiogenesis, platelet activation, complement system, adipokines signaling pathway, peroxisome, cancer pathway, transforming growth factor (TGF) signaling pathway, axon guidance, cell cycle, etc.ConclusionThere are a large number of differentially spliced genes in gastric cancer tissue samples, and the difference in expression due to changes in splice sites may play an important role in the development of gastric cancer.
Objective To summarize the research progress of alternative splicing in pancreatic cancer, and to provide reference for further research. MethodThe experimental and clinical studies of alternative splicing in pancreatic cancer were reviewed.Results Alternative splicing dysregulation resulted in changed gene expression or novel isoform formation, thereby influencing the carcinogenesis, progression or chemoresistance of pancreatic cancer. The differentially expressed alternative splicing isoforms may serve as diagnostic markers, indicators of aggressiveness or prognostic markers of pancreatic cancer. Conclusion Further investigation of the molecular mechanisms of alternative splicing in carcinogenesis and progression of pancreatic cancer is a new way to improve the early diagnosis and treatment of pancreatic cancer.