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作 者:余丹[1] 林菊生[1] 孙昕[1] 叶媛[1] 吴伟[1] 林茂伟[1]
机构地区:[1]华中科技大学同济医学院附属同济医院肝病研究所,湖北武汉430030
出 处:《胃肠病学和肝病学杂志》2009年第3期224-227,共4页Chinese Journal of Gastroenterology and Hepatology
摘 要:目的探讨丝氨酸蛋白激酶Omi/HtrA2在肝癌细胞中在促凋亡基因p53与抑凋亡基因XIAP之间调控机制的研究,并探讨其今后用于靶向治疗的可能性。方法用Western blotting的方法半定量测定4种不同的肝细胞株(L02、HepG2、Hep3B、Huh7)中p53、XIAP、Omi/HtrA2蛋白的表达量,以及使用Omi/HtrA2特异性抑制剂ucf-101后各自的表达量。结果在p53表达不同的细胞株中XIAP蛋白和Omi/HtrA2蛋白的表达也是不同的,p53可上调Omi/HtrA2蛋白表达,下调XIAP蛋白表达。使用ucf-101后,肝癌细胞中XIAP蛋白表达明显上调。结论Omi/HtrA2是p53与XIAP之间凋亡调控作用的信号因子之一,参与细胞凋亡的调控,有可能作为肿瘤细胞凋亡的治疗靶点。Objective To study the regulation mechanism of serine stretch protein kinase Omi/HtrA2 in p53 gene which promoted apoptosis and XIAP gene which inhibited apoptosis in hepatoma carcinoma cells, and to explore the possibility as an new target to liver cancer gene therapy. Methods The expressions of p53, XIAP and Omi/HtrA2 gene in the level of protein were detected by Western blotting before and after received specific inhibitor ucf-101 in four liver cancer cell lines L02, HepG2, Hep3B and Huh7. Results The expression of Omi/HtrA2 protein was different in those liver cancer cell lines which the expression of p53 protein was different, p53 gene could up-regulate the expression of Omi/HtrA2 in the level of protein, and then down-regulated the expression of XIAP protein. The XIAP protein was upregulated obviously after received ucf-101 in those liver cancer cell lines. Conclusion Omi/HtrA2 is one of the signal factors between p53 and XIAP, which plays an important role in the regulation to apoptosis of tumor cells. It may be a new therapy target to liver cancer gene therapy.
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