IGF2-AS knockdown inhibits glycolysis and accelerates apoptosis of gastric cancer cells through targeting miR-195/CREB1 axis.

Dysregulation of long non-coding RNA (lncRNA) insulin growth factor 2 antisense (IGF2-AS) is being found to have relevance to tumorigenesis, including gastric cancer (GC). The purpose of this study was to further explore the detailed role and molecular mechanism of IGF2-AS in GC progression. The expression levels of IGF2-AS, miR-195 and cAMP responsive element binding protein 1 (CREB1) mRNA were assessed by qRT-PCR. Glucose consumption and lactate production were determined using a corresponding Commercial Assay Kit. Hexokinase 2 (HK2) and CREB1 protein levels were detected using western blot. Cell apoptosis was determined by flow cytometry. The targeted interaction between miR-195 and IGF2-AS or CREB1 was validated using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Our data revealed that IGF2-AS was upregulated in GC tissues and predicted poor prognosis. IGF2-AS knockdown hampered glycolysis and accelerated apoptosis of GC cells. Moreover, IGF2-AS acted as a sponge of miR-195 and CREB1 was a direct target of miR-195. MiR-195 mediated the regulatory effect of IGF2-AS knockdown on GC cell glycolysis and apoptosis. MiR-195 exerted its regulatory effect on GC cell glycolysis and apoptosis by CREB1. Furthermore, IGF2-AS regulated CREB1 expression via sponging miR-195. In conclusion, our study suggested that IGF2-AS knockdown suppressed glycolysis and facilitated apoptosis in GC cells at least partly through sponging miR-195 and modulating CREB1 expression, highlighting a novel therapeutic strategy for GC treatment.