Kim Tae Woo
Department of Biopharmaceutical Engineering, Dongguk University-WISE, 123 Dongdae-ro, Gyeongju 38066, Gyeongbuk, Republic of Korea.
Antioxidants (Basel). 2023 Feb 15;12(2):492. doi: 10.3390/antiox12020492.
exerts powerful anti-tumor and anti-cancer effects in various cancer cell types. However, there have been few studies regarding the anti-cancer effect of nodakenin, a bioactive compound of , in vivo and in vitro on breast cancers. I found that nodakenin, in a concentration-dependent manner, inhibits breast cancer cell viability and decreases the tumor volume in mice. Additionally, nodakenin induces caspase-3-dependent apoptosis in breast cancer cells; however, the combination of Z-VAD-FMK and nodakenin suppresses the caspase-3-dependent apoptotic cell death. Furthermore, nodakenin mediates apoptotic cell death via the PERK-mediated signaling pathway and calcium (Ca) release, and nodakenin combined with thapsigargin induces synergistic cell death by inhibiting sarco/endoplasmic reticulum (ER) Ca-ATPase. However, knockdown of PERK or CHOP inhibits Ca generation and caspase-dependent apoptosis in nodakenin-treated breast cancer cells. Nodakenin induces ROS and Ca generation, ER stress, and apoptotic cell death; however, the knockdown of Nox4 inhibits ROS generation and ER stress- and caspase-dependent apoptotic cell death. In addition, nodakenin combined with radiation overcomes radioresistance in radioresistant breast cancer cells by suppressing epithelial-mesenchymal transition phenotypes, including the decrease in E-cadherin and the increase in N-cadherin and vimentin. Therefore, these findings indicate that nodakenin may be a novel therapeutic strategy for breast cancers.
在多种癌细胞类型中发挥强大的抗肿瘤和抗癌作用。然而，关于[此处原文缺失相关信息]的生物活性化合物紫花前胡苷元在体内和体外对乳腺癌的抗癌作用的研究很少。我发现紫花前胡苷元以浓度依赖的方式抑制乳腺癌细胞活力并减小小鼠肿瘤体积。此外，紫花前胡苷元诱导乳腺癌细胞中依赖半胱天冬酶 - 3的凋亡；然而，Z - VAD - FMK与紫花前胡苷元的组合抑制了依赖半胱天冬酶 - 3的凋亡性细胞死亡。此外，紫花前胡苷元通过PERK介导的信号通路和钙（Ca）释放介导凋亡性细胞死亡，并且紫花前胡苷元与毒胡萝卜素联合通过抑制肌浆网/内质网（ER）Ca - ATP酶诱导协同性细胞死亡。然而，敲低PERK或CHOP可抑制紫花前胡苷元处理的乳腺癌细胞中的钙生成和半胱天冬酶依赖性凋亡。紫花前胡苷元诱导活性氧（ROS）和钙生成、内质网应激以及凋亡性细胞死亡；然而，敲低Nox4可抑制ROS生成以及内质网应激和半胱天冬酶依赖性凋亡性细胞死亡。此外，紫花前胡苷元与放疗联合通过抑制上皮 - 间质转化表型（包括E - 钙黏蛋白减少以及N - 钙黏蛋白和波形蛋白增加）克服了耐辐射乳腺癌细胞的放射抗性。因此，这些发现表明紫花前胡苷元可能是一种针对乳腺癌的新型治疗策略。
