Overexpression Of BASP1 Confers A Poor Prognosis In Gastric Cancer

Background:Gastric cancer(GC)is currently one of the most frequently diagnosed cancers with high mortality rates worldwide.Patients with stage I gastric cancer(SIGC)have a good prognosis,however,some patients develop recurrence and metastasis within a short time frame.Based on SIGC patients with indications of early T and N stages but no distant metastasis,it is essential to develop novel biomarkers for prognosis and to understand the underlying molecular mechanisms response for progression.Weighted gene co-expression network analysis(WGCNA)is a method to jointly analyze clinical information and gene expression data.Extensive publicly available genomic and clinical data can be obtained from the Cancer Genome Atlas(TCGA).Currently,based on WGCNA and TCGA datasets,researchers have gained further understanding of the molecular mechanisms and characteristics of various cancers.Methods:Clinical data from SIGC patients in TCGA were analyzed by WGCNA.In the black gene module highly related to the clinical classification of Grade differentiation,we screened TOP 25 hub genes.Survival analysis was performed to identify genes affecting SIGC prognosis.In addition,the effects of these genes on the prognosis of SIGC were confirmed by cytological experiments.We further explored the mechanism by which this gene affects the prognosis of GC through gene set enrichment analysis(GSEA).Results:330 samples were analyzed from TCGA,which included 51 SIGC samples.In the TOP 25 hub genes,OS(Overall Survival)in patients with high expression of BASP1(brain acid soluble protein 1)was shorter than those with low expression of BASP1(p = 0.01625).Cytological analysis showed the proliferation ability of GC cell lines after knockdown of BASP1 did not show significant change and the migration ability decreased by 62.2%.GSEA indicated that the IL6-JAK-STAT3 pathway was highly enriched(NOM p-val = 0.000;FDR q-val = 0.000).Conclusion:BASP1 is a poor prognostic factor for SIGC which may impact the cell migration of GC through regulation of the IL6-JAK-STAT3 pathway.