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Sci Rep:海南医学院李孟森研究组发表甲胎蛋白生物学功能生物学功能研究成果

摘要 : 2016年6月3日,国际学术权威刊物自然出版集团旗下子刊《Scientific Reports》杂志在线发表了海南医学院李孟森研究员团队题为《Alpha fetoprotein antagonized apoptosis induced by paclitaxel of hepatoma cells in vitro》的论文。

 2016年6月3日,国际学术权威刊物自然出版集团旗下子刊《Scientific Reports》杂志在线发表了海南医学院李孟森研究员团队题为《Alpha fetoprotein antagonized apoptosis induced by paclitaxel of hepatoma cells in vitro》的论文。论文研究结果显示,肝癌细胞高表达的AFP具有对抗紫杉醇诱导的肝癌细胞凋亡,发现AFP肝癌细胞耐药的新靶点,同时也发现AFP是一个促进肝癌转移、耐药的关键分子。李孟森PI团队成员朱明月、李伟和鲁琰为论文共同第一作者,李孟森和郭峻莉为通信作者。

论文均以AFP的生物学功能为研究中心,研究结果显示,肝癌细胞高表达的AFP具有对抗紫杉醇诱导的肝癌细胞凋亡,AFP通过抑制caspase-3活性和促进肝癌细胞Ras和Survivin表达,导致肝癌细胞耐受紫杉醇的作用,发现肝癌细胞在耐受紫杉醇诱导凋亡过程中,形成具有癌干细胞特性的细胞。研究结果也显示,乙型肝炎病毒-X蛋白(HBx)优先驱动AFP表达促进肝癌细胞耐药和驱动癌细胞转移,证明AFP是一个促进肝癌发生、癌细胞转移和耐药的关键分子。靶向抑制AFP表达能促进肝癌细胞对药物的敏感性,同时也能抑制肝癌细胞的转移。这些研究结果进一步证明,AFP表达是HBx诱导肝癌发生的重要环节,也确定了AFP是促进癌恶性行为的重要分子。

《Scientific Reports》杂志评审专家给予相当高的评价:这篇论文是一个好的构思和施行一系列的实验来证明AFP涉及肝癌细胞侵袭和转移的密切关系。作者已经使用高端技术,尖端的方法证明他们的设想,他们的结果能清楚的证明AFP在促进肝癌细胞转移发挥关键性作用。这个设想具有较大的原创性,较好的执行研究计划。

原文链接:

Alpha fetoprotein antagonizes apoptosis induced by paclitaxel in hepatoma cells in vitro

原文摘要:

Hepatocellular carcinoma (HCC) cell resistance to the effects of paclitaxel has not been adequately addressed. In this study, we found that paclitaxel significantly inhibited the viability of HLE, Bel 7402 and L-02 cells in a dose- and time-dependent manner. HLE cells and L-02 cells resisted the cytotoxicity of paclitaxel when transfected with pcDNA3.1-afp vectors. However, Bel 7402 cell sensitivity to paclitaxel was increased when transfected with alpha fetoprotein (AFP)-siRNA. Bel 7402 cell resistance to paclitaxel was associated with the expression of the “stemness” markers CD44 and CD133. Paclitaxel significantly inhibited growth and promoted apoptosis in HLE cells and L-02 cells by inducing fragmentation of caspase-3 and inhibiting the expression of Ras and Survivin, but pcDNA3.1-afpvectors prevented these effects. However, paclitaxel could not significantly promote the cleavage of caspase-3 or suppress the expression of Ras and Survivin in Bel 7402 cells. Silenced expression of AFP may be synergistic with paclitaxel to restrain proliferation and induce apoptosis, enhance cleavage of caspase-3, and suppress the expression of Ras and Survivin. Taken together, AFP may be an important molecule acting against paclitaxel-inhibited proliferation and induced apoptosis in HCC cells via repressing the activity of caspase-3 and stimulating the expression of Ras and Survivin. Targeted inhibition of AFP expression after treatment with paclitaxel is an available strategy for the therapy of patients with HCC.

来源: Scientific Reports 浏览次数:0

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