Formononetin Inhibits Non-Small Cell Lung Cancer Proliferation via Regulation of mir-27a-3p through p53 Pathway

Objective: The aim of the present study was to investigate the anti-tumor effects of formononetin on human nonsmall cell lung cancer (NSCLC) and its potential molecular mechanism. Methods: A549 cells were treated withdifferent concentrations of formononetin, then detected the cell proliferation, apoptosis and the expression ofHIPK2 respectively by MTT assay, flow cytometry analysis and RT-qPCR. Then the interaction between miR-27a-3p and its target gene HIPK2 was verified through luciferase reporter assay. The expression of miR-27a-3p, HIPK2, and p53 was detected after being treated with different formononetin concentrations by RT-qPCRand western blot. Results: The results showed that formononetin significantly inhibited the proliferation andinduced the apoptosis of A549 cells in a time- and dose-dependent manner. miR-27a-3p targeted HIPK23’UTR and inhibited the expression of HIPK2. Also, formononetin-treated A549 cells were remarked with asignificant decline in the expression of miR-27a-3p, accompanied with growth of HIPK2, and subsequently areduction of p53. Conclusions: The study indicates that miR-27a-3p might pose regulated effects on theHIPK2/p53 pathway, resulting in formononetin’s anti-carcinogenic effects on NSCLC in vitro.