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人癌胚抗原作为失巢凋亡的一般抑制剂发挥作用。

Human carcinoembryonic antigen functions as a general inhibitor of anoikis.

作者信息

Ordoñez C, Screaton R A, Ilantzis C, Stanners C P

机构信息

McGill Cancer Centre and Department of Biochemistry, McGill University, Montreal, Quebec, Canada.

出版信息

Cancer Res. 2000 Jul 1;60(13):3419-24.

Abstract

Human carcinoembryonic antigen (CEA), a widely used tumor marker, and CEACAM6 [formerly nonspecific cross-reacting antigen (NCA)] are up-regulated in many types of human cancers, whereas family member CEACAM1 [formerly biliary glycoprotein (BGP)] is usually down-regulated. Deregulated overexpression of CEA/CEACAM6 but not CEACAM1 can inhibit the differentiation and disrupt the polarization and tissue architecture of many different types of cells. In this report, we show that CEA and CEACAM6, but not CEACAM1, markedly inhibit the apoptosis of cells when deprived of their anchorage to the extracellular matrix, a process known as anoikis. By blocking this tissue architecture surveillance mechanism, the architectural perturbation initiated by CEA/CEACAM6 can thus be maintained.

摘要

人癌胚抗原(CEA)是一种广泛应用的肿瘤标志物,而癌胚抗原相关细胞黏附分子6(CEACAM6)[原非特异性交叉反应抗原(NCA)]在多种人类癌症中表达上调,而其家族成员癌胚抗原相关细胞黏附分子1(CEACAM1)[原胆汁糖蛋白(BGP)]通常表达下调。CEA/CEACAM6而非CEACAM1的失调过表达可抑制多种不同类型细胞的分化,并破坏其极化和组织结构。在本报告中,我们表明,CEA和CEACAM6而非CEACAM1,在细胞脱离细胞外基质锚定(一种称为失巢凋亡的过程)时,能显著抑制细胞凋亡。通过阻断这种组织结构监测机制,由CEA/CEACAM6引发的结构扰动得以维持。

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