Figure 3.

BMSC‐EV‐derived let‐7i represses KDM3A to further inhibit the development of lung cancer. A, RAID, mirDIP, DIANA TOOLS, miRDB, starBase and miRWalk were used to predict the downstream genes of let‐7i and Venn diagrams were plotted to take intersections. B, Venn diagram of human transcription obtained from let‐7i downstream genes and Cistrome Factor and the intersection gene is KDM3A. C, The binding site of let‐7i and KDM3A predicted by starBase. D, The relationship between let‐7i and KDM3A verified by dual‐luciferase reporter gene assay. E, The expression of KDM3A in lung cancer tissues determined by RT‐qPCR (n = 65), *P < .05 compared with paracancerous tissues. F, The expression of KDM3A in lung cancer cells A549 and normal human lung fibroblasts LL29 measured by RT‐qPCR, *P < .05 compared with LL29. G, The expression of KDM3A in lung cancer cells treated with EVs determined by RT‐qPCR, *P < .05 compared with cells treated by BMSC‐EVs. H‐I, The expression of let‐7i and KDM3A in lung cancer cells transfected with oe‐KDM3A treated by EVs measured by RT‐qPCR. *P < .05 compared with cells transfected with oe‐NC, #P < .05 compared with cells transfected with oe‐KDM3A; & P < .05 compared with cells transfected with KDM3A + EV‐inhibitor‐NC. J, The proliferation ability of lung cancer cells treated with EVs determined by CCK‐8, *P < .05 compared to cells transfected with oe‐NC; #P < .05 compared to cells transfected with oe‐KDM3A; & P < .05 compared to cells transfected with oe‐KDM3A + EV‐inhibitor‐NC. K, The migration and invasion of lung cancer cells determined by Transwell (× 200), *P < .05 compared with cells transfected with oe‐NC; #P < .05 compared with cells transfected with oe‐KDM3A; &P < .05 compared with cells transfected with oe‐KDM3A + EV‐inhibitor‐NC. The experiments were repeated 3 times