Fig. 3

MiR-130b inhibition attenuates lung cancer cell aggressiveness via PPARγ/VEGF-A/BCL-2-mediated enhancement of apoptosis. a Representative images of A549 cells treated with anti-miR-130b and co-labeled for PPARγ (green) and VEGF-A (red) (scale bar, 50 μm). b Representative images of A549 cells treated with anti-miR-130b and labeled for BCL-2 (green) (scale bar, 50 μm). c and d Anti-miR-130b increased PPARγ, but decreased VEGF-A and BCL-2. e MiR-130b and its putative binding sequence in the PPARγ 3'-UTR. The mutant PPARγ binding site was generated in the complementary site for the seed region of miR-130b. Anti-miR-130b caused a significant increase in the luciferase activity of wt 3'-UTR of PPARγ. f A slower proliferation rate in cells treated with anti-miR-130b compared with controls. g Decreased number of invaded cells with anti-miR-130b treatment (scale bar, 100 μm). h Shorter migrated distance in cells treated with anti-miR-130b at indicated time points. i Decreased colonies in cells treated with anti-miR-130b at 48 hours time point. j Increased apoptotic cells treated with anti-miR-130b compared with controls. k Increased apoptotic rate in cells treated with anti-miR-130b (scale bar, 50 μm). Anti-MC: anti-miR-130b control; anti-M: anti-miR-130b; TUNEL, terminal deoxynucleotidyl transferase-mediated uridine 5’-triphosphate-biotin nick end labeling; UTR, untranslated region; wt, wild type; mt, mutant type. Each bar represents the mean ± SD. Results are representative of three independent experiments. *p < 0.05, #p < 0.001