Magnolol induces apoptosis in osteosarcoma cells via G0/G1 phase arrest and p53-mediated mitochondrial pathway
Magnolol induces apoptosis in osteosarcoma cells via G0/G1 phase arrest and p53-mediated mitochondrial pathway
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DOI：
10.1002/jcb.28968
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发表时间：
2019-10-01
影响因子：
4
通讯作者：
Li, Haohuan
中科院分区：
文献类型：
--
作者：
Zhou, Siqi;Wen, Haiyan;Li, Haohuan
骨肉瘤是一种高度侵袭性的原发性骨恶性肿瘤。厚朴酚具有生物活性，在多种癌细胞系中显示出抗肿瘤作用。然而，厚朴酚对人骨肉瘤细胞（HOC）的作用尚不清楚。本研究旨在确定厚朴酚的抗肿瘤活性，并阐明其在HOC中的分子机制。厚朴酚对MG-63和143 B细胞的生长有明显的抑制作用，并诱导细胞凋亡，使细胞周期阻滞于G 0/G1期。在骨肉瘤细胞中，厚朴酚上调促凋亡蛋白的表达，抑制抗凋亡蛋白的表达。此外，在pifithrin-a（PFT-a，p53抑制剂）的预处理下，木兰酚诱导的凋亡被显著逆转。以上结果表明，木兰醇可能通过G 0/G1期阻滞和p53介导的线粒体途径诱导骨肉瘤细胞凋亡。
Osteosarcoma is a highly invasive primary malignancy of bone. Magnolol is biologically active, which shows antitumor effects in a variety of cancer cell lines. However, it has not been elucidated magnolol's effects on human osteosarcoma cells (HOC). This study aimed to determine antitumor activity of magnolol and illustrate the molecular mechanism in HOC. Magnolol showed significant inhibition effect of growth on MG-63 and 143B cells and induced apoptosis and cell cycle arrest at G0/G1. In osteosarcoma cells, magnolol upregulated expressions of proapoptosis proteins and suppressed expressions of antiapoptosis proteins. Additionally, under the pretreatment of pifithrin-a (PFT-a, a p53 inhibitor), the magnolol-induced apoptosis was significantly reversed. The results above indicated that magnolol induces apoptosis in osteosarcoma cells may via G0/G1 phase arrest and p53-mediated mitochondrial pathway.