Dihydromyricetin Reduces TGF-β Via P53 Activation-dependent Mechanism in Hepatocellular Carcinoma HepG2 Cells
Dihydromyricetin Reduces TGF-β Via P53 Activation-dependent Mechanism in Hepatocellular Carcinoma HepG2 Cells
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DOI：
10.2174/0929866524666170223143113
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发表时间：
2017-01-01
影响因子：
1.6
通讯作者：
Zhu, Runzhi
中科院分区：
文献类型：
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作者：
Huang, Xiaojie;Lian, Tianming;Zhu, Runzhi
天然抗肿瘤药物的开发是临床肿瘤治疗的关键。从显齿蛇葡萄茎叶中提取了具有生物活性的黄酮类化合物二氢杨梅素。根据我们以前的研究，它具有抗癌活性，并诱导人肝癌细胞凋亡。本研究采用MTT法和流式细胞仪检测DHM对HepG 2细胞的增殖抑制作用和诱导凋亡作用。我们发现DHM可以调节TGF-β信号通路，并与P53、Smad 3和P-Smad 2/3蛋白存在交叉作用。同时，我们证实DHM通过调节p53依赖性通路（MDM 2、P-MDM 2、BAX和Bcl-2）的激活而显示出抗肿瘤活性。这些发现定义并支持DHM通过p53信号通路降低TGF-β诱导HepG 2细胞凋亡的新机制。
Natural antineoplastic drug development is crucial to treatment of clinical oncology. Di-hydromyricetin, a bioactive flavonoid compound was extracted from the stems and leaves of Ampelopsis grossedentata. It exhibited anticancer activity and induced apoptosis in human hepatocellular carcinoma cells according to our previous studies. In this study, we demonstrated that DHM could significantly inhibit proliferation and induce apoptosis in HepG2 cells with MTT and Flow Cytometry methods. It is very interesting that we found DHM could regulate TGF-beta signal pathway and which has a crosstalk with P53, Smad3 and P-Smad2/3 proteins. Meanwhile, we confirmed that DHM showed antitumor activity by regulating the activation of the p53-dependent pathways (MDM2, P-MDM2, BAX and Bcl-2). These findings defined and supported a novel mechanism that DHM could induce cell apoptosis by reducing TGF-beta via p53 signal pathway in HepG2 cells.