Abstract
Higher methylation levels of RNA-binding protein for multiple splicing 2 (RBPMS2) was reported to be related with unfavorable outcome in gastric cancer (GC). However, molecular function and diagnostic significance of DNA methylation of RBPMS2 remains indistinct. Here we aimed to whether DNA methylation of RBPMS2 acts as a diagnosis biomarker in GC pathogenesis and its potential clinical significance. Western blot and immunochemistry assays were carried out to explore the level of RBPMS2. GC malignancy behaviors were determined by cell counting kit-8, Transwell, flow cytometry analysis and terminal-deoxynucleoitidyl transferase mediated nick end labeling staining. The inflammatory cell infiltration in xenograft model was observed by hematoxylin and eosin staining. CpG Islands was predicted by MethPrimer and the DNA methylation of RBPMS2 was evaluated by methylation-specific polymerase chain reaction. The results showed that RBPMS2 was downregulated in GC specimens. Poor survival rates were associated with low RBPMS2 expression. Overexpression of RBPMS2 inhibited GC growth while facilitated apoptosis in GC cells. In addition, level of DNA methylation of RBPMS2 in GC tissues was increased and DNA methylation of RBPMS2 was strongly associated with tumor invasion, Borrmann classification and TNM stage. We also observed that DNA methylation inhibitors counteracted the role of RBPMS2 in restraining GC development and tumorigenesis. To sum, our data demonstrated that DNA methylation of RBPMS2 was responsible for its downregulation in GC and promoted tumor progression, indicating DNA methylation of RBPMS2 might serve as a valuable potential parameter in GC pathogenesis.