Naringin inhibits thyroid cancer cell proliferation and induces cell apoptosis through repressing PI3K/AKT pathway.

The present study aimed to investigate the anti-tumor effects of naringin in thyroid cancer (TC), and to explore the underlying mechanisms. TC cell lines TPC-1 and SW1736 were treated with 6, 12 or 25 μg/ml naringin for indicated times. Then, cell proliferation was determined using 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay, and cell apoptosis was analyzed by flow cytometer. Moreover, cell proliferation and apoptosis related genes (cyclin D1, c-Myc, survivin, Caspase3, Bcl-2, and Bax) were measured by western blot assay and quantitative reverse transcription-polymerase chain reaction (qRT-PCR) respectively. Cleaved Caspase3 was measured using western blot assay. Phosphatidylinositol 3-kinase (PI3K)/AKT pathway was also analyzed in this study. Results indicated that naringin dose- and time-dependently inhibited TPC-1 and SW1736 cell proliferation, and naringin dose-dependently induced TPC-1 and SW1736 cell apoptosis. In addition, we found that naringin dose-dependently enhanced the expression of Caspase3, cleaved Caspase3 and Bax, and reduced the expression of cyclin D1, c-Myc, survivin, and Bcl-2 in TPC-1 and SW1736 cells. Moreover, we found that naringin dose-dependently suppressed PI3K/AKT pathway activation in TC cells. In conclusion, the data of this study suggested that naringin presented anti-tumor effects in TC cells through inhibiting TC cell proliferation and inducing cell apoptosis via regulating the expression of cell proliferation and apoptosis related genes and PI3K/AKT pathway activation. Our study suggested the potential value of naringin in the treatment of TC and provided more theoretical evidence for the treatment of TC.