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活化型高分子量激肽原潜在的抗肿瘤作用及其分子机制
引用本文:徐秀月,杨威.活化型高分子量激肽原潜在的抗肿瘤作用及其分子机制[J].中国生物化学与分子生物学报,2006,22(9):691-696.
作者姓名:徐秀月  杨威
作者单位:中国医科大学附属二院血液科,沈阳,110004
基金项目:辽宁省教育厅资助项目;辽宁省自然科学基金
摘    要:高分子量激肽原是血浆中一种多功能的糖蛋白,与血液凝固的启动、 补体反应及炎症发生等有密切关系.新近的研究显示,活化型高分子量激肽原 具有潜在的抗肿瘤作用.本文综述活化型高分子量激肽原在细胞粘附和血管 生成中发挥的抑制作用及其活性区域,抑制细胞迁移、增殖并诱导细胞凋亡 的作用,及其在细胞表面的作用位点和分子机制.活化型高分子量激肽原作用 机制,包括抑制细胞DNA的从头合成,使细胞周期蛋白D1表达下降,以及通过 影响细胞内信号通路发挥其活性效应等.深入研究活化型高分子量激肽原在 细胞表面作用的信号转导通路可能是今后抗肿瘤研究途径之一.

关 键 词:高分子量激肽原  细胞粘附  血管生成  细胞迁移和增殖  细胞凋亡  
收稿时间:2006-2-23
修稿时间:2006年2月23日

Potential Anti tumor Function of Cleaved HighMolecular Weight Kininogen and Its Molecular Mechanism
XU Xiu-Yue,YANG Wei.Potential Anti tumor Function of Cleaved HighMolecular Weight Kininogen and Its Molecular Mechanism[J].Chinese Journal of Biochemistry and Molecular Biology,2006,22(9):691-696.
Authors:XU Xiu-Yue  YANG Wei
Institution:DepartmentofHematology,SecondAffiliatedHospital,ChinaMedicalUniversity,Shenyang110004,China
Abstract:High molecular weight kininogen (HK) is a multifunctional glycoprotein that highly associated with many pathophysiological processes, such as initiation of the blood coagulation, activation of the complement system and inflammative reaction. Recent studies indicate that cleaved high molecular weight kininogen (HKa) possesses the potential function of anti tumor. In this review, we summarized the inhibition and active region of HKa in the adhesion of tumor cells and angiogenesis, the inhibition effect in cell migration and proliferation and induce tumor cell apoptosis effect. We also summarized the target which the HKa act on the endothelial cell surface and its molecular mechanism. HKa can inhibite the  de novo synthesized of DNA in proliferating cells,decreases cyclin D1 expression, which is a critical component required for the transition from G1 to S phase of the cell cycle, disrupts intracellular signal pathways. Therefore, further study on the signal transduction pathway of HKa is a challenging task.
Keywords:high molecular weight kininogen  cell adhesion  angiogenesis  cell migration and proliferation  cell apoptosis
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