Fig. 6
ENO1 participated in the oncogenic function of AL355338. A Relative expression levels of AL355338 in A549 and PC9 cells transfected with pcDNA-AL355338. B Western blot analysis showed stable downregulation of ENO1 by sh-ENO1 in A549 and PC9 cells. C–E CCK-8, colony formation and EdU assays demonstrated that knockdown of ENO1 partially attenuated the enhanced cell proliferation induced by overexpression of AL355338 in A549 and PC9 cells. Scale bar = 100 μm (colony) or 50 μm (EdU). F Cell migration and invasion were detected by transwell assays to assess the impact of ENO1 silencing on the role of AL355338 overexpression. Scale bar, 50 μm. G The effect of AL355338 downregulation on the protein levels of E-cadherin was rescued by ENO1 knockdown, while the upregulation of N-cadherin and Vimentin was reduced. H, I Metabolic functional rescue experiments showed that 18F-FDG uptake and lactate production promoted by ectopic expression of AL355338 could be repressed by sh-ENO1 in A549 and PC9 cells. Data shown are mean ± SD (n = 3) (*P < 0.05, **P < 0.01, ***P < 0.001)