Fig. 7

EZH2 was responsible for ANLN-induced pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis. a, EZH2 downregulation significantly inhibited the expression of LASP1 protein in BxPC-3 and SW1990 cells. b, MiR-218-5p inhibitor (anti-miR-218) obviously reversed the EZH2 knockdown-induced miR-218-5p expression. c, The LASP1 protein levels were partly restored in the cells cotransfected with EZH2 RNAi and anti-miR-218 compared with the protein levels in the cells cotransfected with EZH2 RNAi and inhibitor control (anti-con). b, EZH2 re-expression obviously reversed the ANLN knockdown-induced miR-218-5p expression. e, EZH2 re-expression obviously reversed the expression levels of LASP1 protein impaired by ANLN knockdown. f, CCK-8 analysis revealed that ectopic expression of EZH2 reversed the inhibition of cell proliferation in BxPC-3 and SW1990 cells transfected with ANLN RNAi. g, Partial restoration of the suppressed cell growth was observed by colony formation after LASP1 re-expression. h, Ectopic expression of EZH2 in BxPC-3 and SW1990 cells partly reversed the suppressive effects of ANLN knockdown in migration and invasion. **P < 0.01