Depletion of miR‐27a up‐regulates BTG2 to restrain cell proliferation and invasion and to promote apoptosis in PC. A and B, Positive cell proliferation in PC after the treatment of BTG2 plasmid and the co‐treatment of miR‐27a mimic and BTG2 plasmid detected by EdU (200×). C and D, Cell invasion in PC after the treatment of BTG2 plasmid and the co‐treatment of miR‐27a mimic and BTG2 plasmid (200×). E and F, Cell apoptosis in PC after the treatment of BTG2 plasmid and the co‐treatment of miR‐27a mimic and BTG2 plasmid. G and H, Protein levels of VEGF, VEGFR, MMP‐2 and MMP‐9 after the treatment of BTG2 plasmid and the co‐treatment of miR‐27a mimic and BTG2 plasmid. *P < .05 vs PANC‐1 cells treated with BTG2‐NC or both miR‐27a mimic and BTG2. The above data are measurement data and described as mean ± standard deviation. Comparisons among multiple groups are analysed by one‐way analysis of variance. The experiment was repeated 3 times independently. miR‐27a, microRNA‐27a; BTG2, B‐cell translocation gene 2; PC, pancreatic cancer; NC, negative control; EdU, 5‐ethynyl‐2’‐deoxyuridine; VEGF, vascular endothelial growth factor; VEGFR, vascular endothelial growth factor receptor; MMP, matrix metallopeptidase