ARHGAP11A is a potential prognostic biomarker and therapeutic target for pancreatic adenocarcinoma

Abstract

The prognosis of pancreatic adenocarcinoma remains dismal up to now, partly owing to a lack of clinically feasible therapeutic targets. ARHGAP11A, a member of Rho GTPase-activating proteins family, has been reported as a prognostic biomarker and oncogene for multiple cancers. However, the specific effects of ARHGAP11A in pancreatic adenocarcinoma remain obscure. In this study, we explored and validated the oncogenic role of ARHGAP11A in pancreatic adenocarcinoma via thorough bioinformatics analyses of public databases and our own RNA-seq data, and in vitro experiments. We found that ARHGAP11A was significantly upregulated in pancreatic adenocarcinoma and correlated with poor clinical outcomes of pancreatic adenocarcinoma patients. Functional enrichment analyses revealed that ARHGAP11A-related genes were enriched in pathways of cell cycle and cell apoptosis. Further molecular functional experiments on ARHGAP11A knockdown pancreatic adenocarcinoma cell lines demonstrated that ARHGAP11A knockdown significantly inhibited cell proliferation, promoted cell cycle arrest in the G1/S stage, and induced cell apoptosis. In comparison, overexpression of ARHGAP11A could remarkably promote the proliferation, cell cycle progression, and apoptosis resistance of pancreatic adenocarcinoma cells. In conclusion, our study demonstrates that ARHGAP11A plays an oncogenic role in pancreatic adenocarcinoma, thus providing a novel therapeutic target and prognostic biomarker for patients with pancreatic adenocarcinoma.