Xanthohumol inhibits cell proliferation and induces apoptosis in human thyroid cells

Abstract

The cell growth inhibitory potential of xanthohumol (XN), a natural prenylflavonoid present in hops and beer, on human papillary thyroid cancer cells is reported. We demonstrate that XN decreases the proliferation of TPC-1 cancer cells in a dose and time dependent manners. At low concentration (10 μM) XN was shown to significantly inhibit carcinogenesis by a mechanism that stops or slows down cell division, preserving the viability of the cells. At higher concentration (100 μM) a decrease of cell viability was observed by induction of apoptosis. As evidenced, XN induced DNA fragmentation in TPC-1 cells and promoted cell cycle arrest, which decreased the percentage of cells in G1 phase and increased in S phase after 72 h of treatment. Furthermore, XN exposure triggered an increase in caspase-3 and caspase-7 activity, supporting its role in the activation of apoptosis. Cell-free studies demonstrated that high concentrations of XN are responsible for an increase of free radicals generated in a Fenton system which may mediate apoptosis through a pro-oxidant pathway. Altogether, our data show that XN induces the apoptosis of TPC-1 cancer cells in a concentration-dependent manner, suggesting XN to be a promising candidate for thyroid cancer therapy.

Keywords: Apoptosis; Prenylchalcone; TPC-1 cell line; Thyroid cancer; Xanthohumol.