Butein is a biologically active flavonoid isolated from the bark of Rhus verniciflua Stokes, which is known to have therapeutic potential against various cancers. Notably, butein inhibits cancer cell growth by inducing G₂/M phase arrest and apoptosis. Butein-induced G₂/M phase arrest is associated with increased phosphorylation of ataxia telangiectasia mutated (ATM) and Chk1/2, and consequently, with reduced cdc25C levels. In addition, butein-induced apoptosis is mediated through the activation of caspase-3, which is associated with changes in the expression of Bcl-2 and Bax proteins. Intriguingly, butein sensitizes cells to tumor necrosis factor-related apoptosis-inducing ligand-induced apoptosis via ERK-mediated Sp1 activation, which promotes the transcription of specific death receptor 5. Butein also inhibits the migration and invasion of human cancer cells by suppressing nuclear factor-κB- and extracellular signal-regulated kinases 1/2-mediated expression of matrix metalloproteinase-9 and vascular endothelial growth factor. Additionally, butein downregulates the expression of human telomerase reverse transcriptase and causes a concomitant decrease in telomerase activity. These findings provide the basis for the pharmaceutical development of butein. The aim of this review is to provide an update on the mechanisms underlying the anticancer activity of butein, with a special focus on its effects on different cellular signaling cascades.

紫铆花素是生物活性的类黄酮从树皮中分离漆树verniciflua斯托克斯，这是众所周知的具有针对各种癌症的治疗潜力。值得注意的是，butein通过诱导G ₂ / M期阻滞和凋亡来抑制癌细胞的生长。酪蛋白诱导的G ₂/ M期阻滞与共济失调毛细血管扩张突变（ATM）和Chk1 / 2的磷酸化增加有关，因此与降低的cdc25C水平相关。此外，丁酸诱导的凋亡是通过caspase-3的激活来介导的，这与Bcl-2和Bax蛋白表达的变化有关。有趣的是，butein通过ERK介导的Sp1激活使细胞对肿瘤坏死因子相关的凋亡诱导配体诱导的凋亡敏感，从而促进特定死亡受体5的转录。butein还通过抑制核因子来抑制人类癌细胞的迁移和侵袭。 -κB-和细胞外信号调节激酶1/2介导的基质金属蛋白酶9和血管内皮生长因子的表达。此外，酪蛋白下调人端粒酶逆转录酶的表达，并导致端粒酶活性随之降低。这些发现为丁酸的药物开发提供了基础。这篇综述的目的是提供丁酸抗癌活性的潜在机制的更新，特别关注其对不同细胞信号级联反应的影响。