Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.

Lu Z; Ghosh S; Wang Z; Hunter T

首页> 外文期刊>Cancer Cell >Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.

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Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.

机译：EGF对小窝蛋白1功能的下调导致E-钙粘蛋白的丢失，β-catenin的转录活性增加和肿瘤细胞侵袭的增强。

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EGF receptor (EGFR) overexpression correlates with metastasis in a variety of carcinomas, but the underlying mechanisms are poorly understood. We demonstrated that EGF disrupted cell-cell adhesion and caused epithelial-to-mesenchymal transition (EMT) in human tumor cells overexpressing EGFR, and also induced caveolin-dependent endocytosis of E-cadherin, a cell-cell adhesion protein. Chronic EGF treatment resulted in transcriptional downregulation of caveolin-1 and induction of the transcriptional repressor Snail, correlating with downregulation of E-cadherin expression. Caveolin-1 downregulation enhanced beta-catenin-TCF/LEF-1 transcriptional activity in a GSK-3beta-independent manner. Antisense RNA-mediated reduction of caveolin-1 expression in EGFR-overexpressing tumor cells recapitulated these EGF-induced effects and enhanced invasion into collagen gels. We propose that EGF-induced negative regulation of caveolin-1 plays a central role in the complex cellular changes leading to metastasis.

机译：EGF受体（EGFR）的过表达与多种癌的转移相关，但对其潜在机制了解甚少。我们证明，EGF破坏了细胞间粘附，并在人类过度表达EGFR的肿瘤细胞中引起了上皮到间质转化（EMT），并且还诱导了E-钙黏着蛋白（一种细胞间粘附蛋白）的依赖小窝蛋白的内吞作用。慢性EGF处理导致小窝蛋白1的转录下调和转录阻遏物Snail的诱导，与E-钙粘蛋白表达的下调有关。 Caveolin-1下调以独立于GSK-3beta的方式增强了β-catenin-TCF/ LEF-1的转录活性。反义RNA介导的EGFR过表达肿瘤细胞中caveolin-1表达的减少，概括了这些EGF诱导的作用并增强了对胶原凝胶的侵袭。我们建议EGF诱导的caveolin-1负调控在导致转移的复杂细胞变化中起着核心作用。

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《Cancer Cell》 |2003年第6期|共17页
作者
Lu Z; Ghosh S; Wang Z; Hunter T;
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正文语种 eng
中图分类肿瘤学;
关键词
caveolin-1; Epidermal Growth Factor; Neoplasms; Cells; 肿瘤; 细胞;

机译：caveolin-1;Epidermal Growth Factor;Neoplasms;Cells;肿瘤;细胞;

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1. Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion. [J] . Lu Z, Ghosh S, Wang Z, Cancer Cell . 2003,第6期

机译：EGF对小窝蛋白1功能的下调导致E-钙粘蛋白的丢失，β-catenin的转录活性增加和肿瘤细胞侵袭的增强。
2. PTPRK negatively regulates transcriptional activity of wild type and mutated oncogenic beta-catenin and affects membrane distribution of beta-catenin/E-cadherin complexes in cancer cells [J] . Novellino L, De Filippo A, Deho P, Cellular Signalling . 2008,第5期

机译：PTPRK负调节野生型和突变的致癌性β-连环蛋白的转录活性，并影响癌细胞中β-连环蛋白/ E-钙粘蛋白复合物的膜分布
3. PTPRK negatively regulates transcriptional activity of wild type and mutated oncogenic beta-catenin and affects membrane distribution of beta-catenin/E-cadherin complexes in cancer cells [J] . Novellino L, De Filippo A, Deho P, Cellular Signalling . 2008,第5期

机译：PTPRK负调节野生型和突变的致癌性β-连环蛋白的转录活性，并影响癌细胞中β-连环蛋白/ E-钙粘蛋白复合物的膜分布
4. VEGF-Functionalized Integrin-Specific Hydrogels for Increased Stem Cell Proliferation, Vascularization and Regeneration of Critically-sized Bone Defects [C] . Jose R. Garcia, Andres J. Garcia Society for Biomaterials annual meeting and exposition . 2015

机译：VEGF功能的整合素特异性水凝胶可用于增加干细胞的增殖，血管化和临界骨缺损的再生。
5. Loss of insulin-like growth factor II receptor in tumorigenic murine cells: Effects on growth and invasion. [D] . Osipo, Clodia. 2002

机译：致瘤鼠细胞中胰岛素样生长因子II受体的丢失：对生长和侵袭的影响。
6. E-cadherin determines Caveolin-1 tumor suppression or metastasis enhancing function in melanoma cells [O] . L Lobos-González, L Aguilar, J Diaz, -1

机译：E-钙粘着蛋白确定黑素瘤细胞中Caveolin-1肿瘤抑制或转移增强功能
7. Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of β-catenin, and enhanced tumor cell invasion [O] . Lu Zhimin, Ghosh Sourav, Wang Zhiyong, 2003

机译：EGF下调Caveolin-1的功能导致E-钙粘蛋白的丢失，β-catenin的转录活性增加以及肿瘤细胞侵袭的增强

Downregulation of caveolin-1 function by EGF leads to the loss of E-cadherin, increased transcriptional activity of beta-catenin, and enhanced tumor cell invasion.

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