Fig. 2.

HOXC10 inhibition impairs cell growth and metastatic capacity in KRAS-mutant lung cancer cells in vitro. a The colony-formation ability analysis of H441-BM and A549-BM cells transfected with the indicated siRNAs. The relative clonogenic viability was normalized to vehicle-treated control. b The migration ability of H441 and A549 cells transfected with the indicated siRNAs for 48 h were detected by transwell assays. The migrated cells were normalized to vehicle-treated control cells. Scale bars, 50 μm. c The migration ability of H441 and A549 cells transfected with the indicated siRNAs for 48 h were detected by was assessed by the wound healing assay. The migration rate was normalized to vehicle-treated control cells. Scale bars, 100 μm. d, e Ectopically expressed HOXC10 restored the clonogenic growth and migration ability of HOXC10-depleted cells. The relative clonogenic viability (d), and migration ability (e) analysis of indicated cells transfected with the indicated siRNAs. Scale bars, 50 μm. f Apoptosis of indicated cells were detected by flow cytometry. H441-bone and A549-bone cells were transfected with 20 nmol/L siRNAs targeting HOXC10 for 48 h. The apoptosis cells were calculated by normalizing the untreated group as 100%. Data in (a–f) represent the mean ± s.e.m. of three technical replicates, representative of three independent experiments with similar results. Panels (a–e) were performed one-way ANOVA with Tukey’s multiple comparison test, *P < 0.05, **P < 0.01, ***P < 0.001