肿瘤-基质相互作用。整合素与细胞黏附作为乳腺细胞存活和转化的调节因子。
Tumour-stromal interactions. Integrins and cell adhesions as modulators of mammary cell survival and transformation.
作者信息
Chrenek M A, Wong P, Weaver V M
机构信息
Department of Biological Sciences, University of Alberta, Edmonton, Canada.
出版信息
Breast Cancer Res. 2001;3(4):224-9. doi: 10.1186/bcr300. Epub 2001 Jun 14.
Abstract
Stromal-epithelial interactions modulate mammary epithelial cell (MEC) growth and apoptosis by influencing cell adhesion and tissue organization. Perturbations in the mammary stroma and cell adhesion characterize breast tumors and underlie the altered tissue organization, disrupted tissue homeostasis and enhanced survival phenotype of the disease. Apoptosis resistance likely arises during malignant transformation via genetic and epigenetic modification of cell adhesion pathways induced by a changing tissue microenvironment. Acquisition of adhesion-linked survival networks that enhance MEC viability in the absence of basement membrane interactions probably promote malignant transformation, and may render breast tumors sufficiently resistant to exogenous apoptotic stimuli to generate multidrug resistance.
摘要
基质-上皮相互作用通过影响细胞黏附和组织构建来调节乳腺上皮细胞（MEC）的生长和凋亡。乳腺基质和细胞黏附的紊乱是乳腺肿瘤的特征，也是该疾病组织构建改变、组织稳态破坏和生存表型增强的基础。凋亡抗性可能在恶性转化过程中通过组织微环境变化诱导的细胞黏附途径的遗传和表观遗传修饰而产生。在缺乏基底膜相互作用的情况下增强MEC活力的黏附相关生存网络的获得可能促进恶性转化，并可能使乳腺肿瘤对外源性凋亡刺激具有足够的抗性从而产生多药耐药性。
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