Triptonide inhibits metastasis potential of thyroid cancer cells via astrocyte elevated gene-1.

Abstract

BackgroundTriptonide (TN) was recently proved to have anti-tumor effects. The current study explored whether TN inhibited thyroid cancer and the possible underlying mechanism.MethodsMDA-T68 and BCPAP cells were treated by TN. Cell viability, migration and invasion rate were detected by MTT and Transwell. Protein expressions were determined by Western blot and mRNA expressions were detected by Real-time Quantitative PCR (qPCR).ResultsTN at the concentration higher than 50 nmol/L inhibited cell viability, migration and invasion of MDA-T68 and BCPAP cells, and astrocyte elevated gene (AEG-1) expression, was decreased by TN at the concentration higher than 50 nmol/L. Furthermore, AEG-1 overexpression inhibited cell viability, migration and invasion capacity of MDA-T68 and BCPAP cells, while TN reduced AEG-1 expression, and weaken the effect of AEG-1 overexpression on cell viability, migration and invasion capacities. Moreover, TN depressed the increase of matrix metalloproteinase (MMP) 2, MMP9 and N-cadherin expressions caused by AEG-1 overexpression. Meanwhile, E-cadherin expression reduced by AEG-1 overexpression was increased by TN.ConclusionsTN could inhibit the metastasis potential of thyroid cancer cells through inhibiting the expression of AEG-1. Our findings reveal the mechanism of TN in the treatment of thyroid cancer, which should be further explored in the study of thyroid cancer.KeywordsTriptonide; metastasis; thyroid cancer; regulation; drug monomer