PDF(Pubmed)
Abstract：
Treating female canine mammary gland tumors is crucial owing to their propensity for rapid progression and metastasis, significantly impacting the overall health and well-being of dogs. Mitoquinone (MitoQ), an antioxidant, has shown promise in inhibiting the migration, invasion, and clonogenicity of human breast cancer cells. Thus, we investigated MitoQ\'s potential anticancer properties against canine mammary gland tumor cells, CMT-U27 and CF41.Mg. MitoQ markedly suppressed the proliferation and migration of both CMT-U27 and CF41.Mg cells and induced apoptotic cell death in a dose-dependent manner. Furthermore, treatment with MitoQ led to increased levels of pro-apoptotic proteins, including cleaved-caspase3, BAX, and phospho-p53. Cell cycle analysis revealed that MitoQ hindered cell progression in the G1 and S phases in CMT-U27 and CF41.Mg cells. These findings were supported using western blot analysis, demonstrating elevated levels of cleaved caspase-3, a hallmark of apoptosis, and decreased expression of cyclin-dependent kinase (CDK) 2 and cyclin D4, pivotal regulators of the cell cycle. In conclusion, MitoQ exhibits in vitro antitumor effects by inducing apoptosis and arresting the cell cycle in canine mammary gland tumors, suggesting its potential as a preventive or therapeutic agent against canine mammary cancer.
摘要：
治疗女性犬乳腺肿瘤是至关重要的，因为它们倾向于快速进展和转移。显著影响狗的整体健康和福祉。线粒体醌(MitoQ),抗氧化剂,在抑制移民方面表现出了希望，入侵,和人类乳腺癌细胞的克隆形成。因此，我们研究了MitoQ对犬乳腺肿瘤细胞的潜在抗癌特性，CMT-U27和CF41。Mg.MitoQ显著抑制CMT-U27和CF41的增殖和迁移。Mg细胞并以剂量依赖性方式诱导凋亡细胞死亡。此外，用MitoQ治疗导致促凋亡蛋白水平升高，包括cleaved-caspase3,BAX,和磷酸化p53。细胞周期分析显示，MitoQ阻碍了CMT-U27和CF41中G1和S期的细胞进展。Mg细胞。这些发现得到了蛋白质印迹分析的支持，显示裂解的caspase-3水平升高，这是细胞凋亡的标志，细胞周期依赖性激酶（CDK）2和细胞周期蛋白D4的表达降低。总之,MitoQ通过在犬乳腺肿瘤中诱导细胞凋亡和阻止细胞周期而表现出体外抗肿瘤作用。提示其作为预防或治疗犬乳腺癌的潜力。
