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转基因TIMP-1通过损害肝细胞增殖和肿瘤血管生成来抑制猿猴病毒40 T抗原诱导的肝癌发生。

Transgenic TIMP-1 inhibits simian virus 40 T antigen-induced hepatocarcinogenesis by impairment of hepatocellular proliferation and tumor angiogenesis.

作者信息

Martin D C, Sanchez-Sweatman O H, Ho A T, Inderdeo D S, Tsao M S, Khokha R

机构信息

Department of Medical Biophysics, University of Toronto, Ontario Cancer Institute, Canada.

出版信息

Lab Invest. 1999 Feb;79(2):225-34.

Abstract

Tissue inhibitors of metalloproteinases (TIMP) block proteolytic degradation of extracellular matrix and consequently impede tumor invasion and metastasis. In addition, we have previously reported that hepatic TIMP-1 modulation alters the susceptibility of the liver to oncogene (simian virus 40 T-antigen; TAg)-induced tumorigenesis in a double-transgenic mouse model. To identify the cellular processes by which TIMP-1 inhibits hepatocarcinogenesis, we examined the effects of TIMP-1 on four specific events that are important during tumorigenesis: hepatocellular proliferation, apoptosis, the stromal characteristics of the liver, and tumor vascularization. Transgenic mice with elevated or reduced hepatic TIMP-1 expression were bred independently with TAg transgenics. Liver tissue from littermates were analyzed by in situ hybridization with TIMP-1 cDNA probes; gelatin enzymography; immunohistochemistry for proliferating cell nuclear antigen, von Willebrand factor, and collagen type IV; reticulin histochemistry; and collagens type III and IV, laminin, fibronectin, and CD31 immunoblotting. We demonstrate that TIMP-1 overexpression significantly inhibited the proliferation of hepatocytes in TAg mice but did not affect their apoptotic index, the hepatic parenchymal architecture, or extracellular matrix composition, including collagens type III and IV, laminin, and fibronectin. Moreover, the hepatocellular carcinomas formed in TIMP-1-overexpressing mice had significantly reduced tumor vascularization; conversely, tumor vascularization was significantly increased in TIMP-1-reduced livers. These data indicate that TIMP-1 inhibits TAg-induced hepatocarcinogenesis by altering hepatocellular proliferation and tumor vascularization, without any effect on hepatocyte apoptosis and stromal composition. To our knowledge, this is the first in vivo demonstration that genetic modulation of TIMP-1 inhibits cellular proliferation and angiogenesis during hepatocarcinogenesis. This potentially extends the use of matrix metalloproteinase inhibitors in cancer beyond control of invasion and metastasis.

摘要

金属蛋白酶组织抑制剂(TIMP)可阻止细胞外基质的蛋白水解降解,从而抑制肿瘤侵袭和转移。此外,我们之前曾报道,在双转基因小鼠模型中,肝脏TIMP-1调节会改变肝脏对癌基因(猿猴病毒40 T抗原;TAg)诱导的肿瘤发生的易感性。为了确定TIMP-1抑制肝癌发生的细胞过程,我们研究了TIMP-1对肿瘤发生过程中四个重要的特定事件的影响:肝细胞增殖、细胞凋亡、肝脏的基质特征以及肿瘤血管生成。将肝脏TIMP-1表达升高或降低的转基因小鼠分别与TAg转基因小鼠杂交。通过用TIMP-1 cDNA探针进行原位杂交、明胶酶谱分析、增殖细胞核抗原、血管性血友病因子和IV型胶原的免疫组织化学、网状纤维组织化学以及III型和IV型胶原、层粘连蛋白、纤连蛋白和CD31免疫印迹分析同窝小鼠的肝脏组织。我们证明,TIMP-1过表达显著抑制了TAg小鼠肝细胞的增殖,但不影响其凋亡指数、肝实质结构或细胞外基质组成,包括III型和IV型胶原、层粘连蛋白和纤连蛋白。此外,在TIMP-1过表达小鼠中形成的肝细胞癌的肿瘤血管生成显著减少;相反,在TIMP-1表达降低的肝脏中,肿瘤血管生成显著增加。这些数据表明,TIMP-1通过改变肝细胞增殖和肿瘤血管生成来抑制TAg诱导的肝癌发生,而对肝细胞凋亡和基质组成没有任何影响。据我们所知,这是首次在体内证明TIMP-1的基因调节在肝癌发生过程中抑制细胞增殖和血管生成。这可能将基质金属蛋白酶抑制剂在癌症中的应用扩展到侵袭和转移控制之外。

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