High expression of collagen 1A2 promotes the proliferation and metastasis of esophageal cancer cells.

Abstract

BackgroundTo undertake a bioinformatics analysis to identify abnormally expressed genes [also referred to as differentially expressed genes (DEGs)] and their functions in esophageal carcinoma (ESCA).MethodsDEGs (i.e., GSE100942, GSE17351, GSE26886, and GSE77861) were obtained from a gene expression omnibus database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using online tools from the Database for Annotation, Visualization and Integrated Discovery. A protein-protein interaction network was then constructed based on the Search Tool for the Retrieval of Interacting Genes website. Cytoscape software was used to identify the top 20 DEGs located in the central region of the network. For the overall survival analysis, a Kaplan–Meier analysis was conducted of the Gene Expression Profiling Interactive Analysis website, and collagen (COL) 1A2 was selected to detect the molecular mechanism of COL1A2-small interfering ribonucleic acid (siRNA) in the following ESCA cell lines: Eca109 and TE-1. Next, the expression of COL1A2-messanger ribonucleic acid was determined using real-time quantitative polymerase chain reaction. The expression of COL1A2 was also verified by Western blot. Cell proliferation was measured by colony-forming and MTT assays, and migration and invasion by the transwell assay.ResultsBased on the GEO database and screening out the hub gene, we identified that COL1A2 was abnormally expressed in ESCA. With a series of in vitro experiments, the expression of COL1A2 was defined as higher in Eca109 and TE-1.ConclusionsCOL1A2 was highly expressed in ESCA tissue samples. Additionally, the proliferation and metastasis of Eca109 and TE-1 cell lines were significantly attenuated by siRNA-COL1A2-mediated small interference. Notably, the expression level of COL1A2 was obviously related to the Akt and epithelial-mesenchymal transition (EMT) pathways.