Isoginkgetin inhibits lung cancer cell progression through miR-27a-5p/APEX1 axis

Abstract

Purpose: To determine the influence of isoginkgetin on the progression of pulmonary carcinogenesis. Methods: A549 cells exposed to isoginkgetin were transfected with miR-27a-5p mimetic and suppressor, as well as short hairpin RNA against apurinic/apyrimidinic endo-deoxyribonuclease 1 (sh-APEX1) for 24 h. Then, the proliferative, migration and invasive potential of A549 cells were determined using CCK-8, wound healing and Transwell assays, respectively. The association between miR-27a-5p and APEX1 was determined by dual-luciferase reporter assay. Results: Isoginkgetin significantly suppressed A549 cell proliferative, migration and invasive activities (p < 0.05). Moreover, isoginkgetin significantly increased miR-27a-5p expression. Furthermore, miR-27a-5p suppressor annulled the influence of isoginkgetin on lung cancer progression. More importantly, the inhibitor directly targeted APEX1, and negatively modulated APEX1 expression (p < 0.05). However, APEX1 knockdown annulled the enhancing effect of miR-27a-5p inhibitor on A549 cell viability, migration and invasion (p < 0.05). Conclusion: Isoginkgetin exerts an anti-lung cancer effect via miR-27a-5p/APEX1 axis. Thus, it is a potential therapy for the management of lung cancer; however, clinical studies are required to validate these findings of this study.