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Previous studies suggest the tumor suppressor role of long non-coding RNA (lncRNA)  STXBP5-AS1  in cervical and gastric cancer, but its expression pattern and functional mechanism are still elusive in pancreatic cancer (PC). Relative expression of  STXBP5-AS1  in PC both in vivo and in vitro was analyzed by real-time PCR. IC 50  of Gemcitabine was determined by the MTT assay. Cell proliferation in response to drug treatment was investigated by colony formation assay. Cell apoptosis was measured by both caspase-3 activity and Annexin V/PI staining. Cell invasion capacity was scored by the transwell assay in vitro, and lung metastasis was examined with the tail vein injection assay. Cell stemness was determined in vitro by sphere formation and marker profiling, respectively, and in vivo by limited dilution of xenograft tumor incidence. Subcellular localization of  STXBP5-AS1  was analyzed with fractionation PCR. Association between  STXBP5-AS1  and  EZH2  was investigated by RNA-immunoprecipitation. The binding of EZH2 on  ADGB  promoter was analyzed by chromatin immunoprecipitation. The methylation was quantified by bisulfite sequencing. We showed downregulation of  STXBP5-AS1  in PC associated with poor prognosis. Ectopic  STXBP5-AS1  inhibited chemoresistance and metastasis of PC cells. In addition,  STXBP5-AS1  compromised stemness of PC cells. Mechanistically,  STXBP5-AS1  potently recruited  EZH2  and epigenetically regulated neighboring  ADGB  transcription, which predominantly mediated the inhibitory effects of  STXBP5-AS1  on stem cell-like properties of PC cells. Our study highlights the importance of the  STXBP5 - EZH2 - ADGB  axis in chemoresistance and stem cell-like properties of PC.

LncRNA STXBP5-AS1 suppresses stem cell-like properties of pancreatic cancer by epigenetically inhibiting neighboring androglobin gene expression