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.

据报道，啤酒花和啤酒中存在的天然异戊二烯类黄酮黄腐酚（XN）对人乳头状甲状腺癌细胞具有潜在的细胞生长抑制作用。我们证明，XN以剂量和时间依赖性方式降低TPC-1癌细胞的增殖。在低浓度（10μM）下，XN已显示出通过停止或减慢细胞分裂的机制显着抑制癌变的机制，从而保持了细胞的活力。在较高浓度（100μM）下，通过诱导细胞凋亡观察到细胞活力降低。如所证明的，XN在TPC-1细胞中诱导DNA片段化并促进细胞周期停滞，这在处理72小时后降低了处于G1期的细胞的百分比并增加了处于S期的细胞。此外，XN暴露触发了caspase-3和caspase-7活性的增加，支持其在凋亡激活中的作用。无细胞研究表明，高浓度的XN导致Fenton系统中产生的自由基增加，而自由基可能通过促氧化剂途径介导细胞凋亡。总之，我们的数据表明XN以浓度依赖的方式诱导TPC-1癌细胞的凋亡，这表明XN是甲状腺癌治疗的有希望的候选者。