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Anti-Tumor Effect of Pinus massoniana Bark Proanthocyanidins on Ovarian Cancer through Induction of Cell Apoptosis and Inhibition of Cell Migration

机译:马尾松树皮原花青素通过诱导细胞凋亡和抑制细胞迁移对卵巢癌的抗肿瘤作用

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摘要

Pinus massoniana bark proanthocyanidins (PMBPs), an active component isolated from Pinus massoniana bark, has been reported to possess a wide range of biochemical properties. Here, we investigated the anti-tumor effect of PMBPs on ovarian cancer. The results indicated that PMBPs significantly reduced the growth of ovarian cancer cells and induced dose-dependent apoptosis. The underlying mechanisms involved were elucidated to include the loss of mitochondrial membrane potential, down-regulation of the anti-apoptotic protein Bcl-2 and the activation of Caspase 3/9, suggesting that PMBPs triggered apoptosis through activation of mitochondria-associated apoptotic pathway. In addition, wound healing and transwell chamber assays revealed that PMBPs could suppress migration and invasion of ovarian cancer cells. PMBPs dramatically inhibited MMP-9 activity and expression, blocked the activity of NFκB and the activation of ERK1/2 and p38 MAPK. Our findings suggest that PMBPs has the potential to be developed as an anti-tumor drug for ovarian cancer treatment and/ or disease management.
机译:马尾松树皮原花色素(PMBPs)是一种从马尾松树皮中分离的活性成分,据报道具有广泛的生化特性。在这里,我们研究了PMBP对卵巢癌的抗肿瘤作用。结果表明,PMBPs显着降低了卵巢癌细胞的生长并诱导了剂量依赖性细胞凋亡。阐明了涉及的潜在机制,包括线粒体膜电位的丧失,抗凋亡蛋白Bcl-2的下调和Caspase 3/9的激活,这表明PMBP通过激活线粒体相关的凋亡途径来触发凋亡。此外,伤口愈合和transwell室分析表明,PMBPs可以抑制卵巢癌细胞的迁移和侵袭。 PMBPs显着抑制MMP-9的活性和表达,阻断NFκB的活性以及ERK1 / 2和p38 MAPK的激活。我们的发现表明,PMBPs有可能被开发为用于卵巢癌治疗和/或疾病管理的抗肿瘤药物。

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