Objective SO AT1 plays an important regulatory role in the occurrence and development of various cancers.However,the biological function and potential molecular mechanism of SOAT1 in gastric cancer(GC)are still unclear.Therefore,we used the data retrieved from the Cancer Genome Atlas(TCGA)and combined with basic experiments to study the role of soatl in gastric cancer.Methods 1.Download the gene expression profile and clinical data of gastric cancer(GC)from the Cancer Genome Atlas(TCGA)database.Difference in SOAT1 expression between normal and cancer tissues was compared by GraphPad software(version7.0)and R software(version 4.0.2).2.qRT-PCR and Western blot were used to investigate the expression of SO AT1 in gastric cancer and adjacent tissues.3.Association between SOAT1 expression and clinicopathologic features was evaluated by Wilcoxon signed-rank test and logistic regression.4.Clinicopathologic characteristics related to overall survival(OS)were determined using the Cox regression and Kaplan-Meier method.5.SO AT1 was down-regulated by siRNA and the cell growth,migration and invasion were detected by cell counting kit-8 assay,wound healing assays and Transwell assays invasion experiments,respectively.6.Further,cellular signaling pathways associated with SO AT1 high expression phenotype were identified by Gene Set Enrichment Analysis(GSEA).Results 1.According to the TCGA database,the expression of SOAT1 in 375 GC tissues was significantly higher than that in 32 non-tumor tissues,and the same results were also presented in matched tissue samples(n=32,p<0.01).Meanwhile,we collected 54 paired tissues and verified that both mRNA and protein expression of SOAT1 was upregulated in GC tissues compared with adjacent normal tissues(p<0.01).2.Besides,the high expression of SOAT1 was related to poor differentiation(p<0.01)and lymph node metastasis(p<0.01).Univariate and multivariate analysis suggested that high SOAT1 expression was an important independent predictor of OS(HR,1.715;95%CI,1.174-2.507;p=0.005)with worse prognosis in GC.3.Cell counting kit-8 assay,wound healing assays and Transwell assays showed that soatl knockout could inhibit the proliferation,migration and invasion of GC cells.4.GSEA showed that Multiple signaling pathways were obviously enriched in samples and associated with high SO AT1 expression phenotype.Conclusion SO AT1 expression was an important independent predictor and knoc kdown of SO AT1 suppressed the proliferation,migration and invasion of GC,wh ich could be a potential prognostic indicator and treatment target. |