This hypothesis was confirmed by further cell-cycle and apoptosis assays, showing that miR-27a-3p inhibition, which consistent with the overexpression of BTG2, induced GC cells G1/S arrest via suppressing cyclinD1 and cyclinE1 protein abundance, and facilitated apoptosis by activating cleaved caspase 3 and PARP1. Here, BTG2 is linked to gastric cancer.