Chang C C, Sun W, Cruz A, Saitoh M, Tai M H, Trosko J E
National Food Safety and Toxicology Center, Department of Pediatrics and Human Development, Michigan State University, East Lansing, Michigan 48824, USA.
Radiat Res. 2001 Jan;155(1 Pt 2):201-207. doi: 10.1667/0033-7587(2001)155[0201:ahbect]2.0.co;2.
Two types of human breast epithelial cells (HBEC) have been characterized. In contrast to Type II HBEC, which express basal epithelial cell phenotypes, Type I HBEC are deficient in gap junctional intercellular communication and are capable of anchorage-independent growth and of expressing luminal epithelial cell markers, estrogen receptors, and stem cell characteristics (i.e. the ability to differentiate into other cell types and to form budding/ductal organoids on Matrigel). A comparative study of these two types of cells has revealed a high susceptibility of Type I HBEC to immortalization by SV40 large T antigen, although both types of cells are equally capable of acquiring an extended life span (bypassing senescence) after transfection with SV40. The immortalization was accompanied by elevation of a low level of telomerase activity in the parental cells after mid-passage ( approximately 60 cumulative population doubling levels). Thus HBEC do have a low level of telomerase activity, and Type I HBEC with stem cell characteristics are more susceptible to telomerase activation and immortalization, a mechanism which might qualify them as target cells for breast carcinogenesis. The immortalized Type I HBEC can be converted to highly tumorigenic cells by further treatment with X rays (2 Gy x 2) and transfection with a mutated ERBB2 (also known as NEU) oncogene, resulting in the expression of p185(ERBB2) which is tyrosine phosphorylated.
已鉴定出两种类型的人乳腺上皮细胞(HBEC)。与表达基底上皮细胞表型的II型HBEC不同,I型HBEC缺乏间隙连接细胞间通讯,能够在不依赖贴壁的情况下生长,并能表达腔上皮细胞标志物、雌激素受体和干细胞特征(即分化为其他细胞类型并在基质胶上形成芽状/导管类器官的能力)。对这两种细胞的比较研究表明,I型HBEC对SV40大T抗原诱导的永生化高度敏感,尽管两种细胞在用SV40转染后都同样能够获得延长的寿命(绕过衰老)。永生化伴随着传代中期(约60个累积群体倍增水平)亲代细胞中低水平端粒酶活性的升高。因此,HBEC确实具有低水平的端粒酶活性,具有干细胞特征的I型HBEC更容易受到端粒酶激活和永生化的影响,这一机制可能使它们成为乳腺癌发生的靶细胞。通过进一步用X射线(2 Gy×2)处理并转染突变的ERBB(2也称为NEU)癌基因,永生化的I型HBEC可以转化为高致瘤性细胞,导致酪氨酸磷酸化的p185(ERBB2)表达。