Apigenin induces c-Myc-mediated apoptosis in FRO anaplastic thyroid carcinoma cells

Apigenin promotes apoptosis in cancer cells. We studied the effect of apigenin on cell survival and c-Myc expression in FRO anaplastic thyroid carcinoma (ATC) cells. Apigenin caused apoptosis via the elevation of c-Myc levels in conjunction with the phosphorylation of p38 and p53. In the c-Myc siRNA-transfected and apigenin-treated cells, compared with the apigenin-treated control cells, apoptosis and phosphorylation of p38 and p53 were ameliorated. In the presence of apigenin, diminution of p38 and p53 did not affect cell survival although apigenin activated the phosphorylation of p38 and p53 via increased c-Myc levels. In conclusion, our results indicate that apigenin induces apoptosis mediated via c-Myc with concomitant phosphorylation of p53 and p38 in FRO ATC cells. These findings suggest that augmented c-Myc acts as a core regulator and is necessary for apigenin-induced apoptosis in FRO ATC cells.

► Apigenin causes cell death in thyroid cancer cells. ► Apigenin augments c-Myc concomitantly with cell death in FRO cells. ► Cell death induced by apigenin is caspase-dependent apoptosis in FRO cells. ► Apigenin-induced apoptosis is mediated through c-Myc in FRO cells. ► Apigenin-induced apoptosis is not directly related to p38 and p53 in FRO cells.