LAUSR

It has previously been reported that glycosylphosphatidylinositol anchor attachment 1 (GPAA1) is overexpressed in hepatocellular carcinoma (HCC); however, its role in regulating the development of HCC remains unknown. The present study aimed to examine the potential role of GPAA1 in HCC and to characterize the associated mechanism. The expression of GPAA1 was first examined using the Gene Expression Profiling Interactive Analysis 2 database, and was then determined using reverse transcription-quantitative PCR and western blotting. The effects of GPAA1 silencing on the proliferation, colony formation, migration and invasion of HuH-7 cells were measured using Cell Counting Kit-8, colony formation, wound healing and Transwell assays, respectively. The interaction between splicing factor (SF)3B4 and GPAA1 was predicted by starBase and confirmed using RNA immunoprecipitation. The results of the present study demonstrated that GPAA1 was upregulated in HCC cells, and silencing GPAA1 markedly inhibited the proliferation, migration and invasion of HCC cells, which was accompanied by reduced levels of MMP2 and MMP9. In addition, it was observed that SF3B4 could bind to GPAA1. Furthermore, to confirm whether SF3B4 binds to GPAA1 to modulate HCC cell behavior, GPAA1 was knocked down and SF3B4 was overexpressed. Overexpression of SF3B4 reversed the effects of GPAA1 knockdown on the proliferation, migration and invasion of HCC cells. In conclusion, SF3B4 may promote the proliferation, invasion and migration of HCC cells by binding to GPAA1. The present study provided novel insight into the pathogenesis of HCC.