Garbe James C, Bhattacharya Sanchita, Merchant Batul, Bassett Ekaterina, Swisshelm Karen, Feiler Heidi S, Wyrobek Andrew J, Stampfer Martha R
Life Sciences Divisions, Lawrence Berkeley National Laboratory, Berkeley, California, USA.
Cancer Res. 2009 Oct 1;69(19):7557-68. doi: 10.1158/0008-5472.CAN-09-0270. Epub 2009 Sep 22.
Normal human epithelial cells in culture have generally shown a limited proliferative potential of approximately 10 to 40 population doublings before encountering a stress-associated senescence barrier (stasis) associated with elevated levels of cyclin-dependent kinase inhibitors p16 and/or p21. We now show that simple changes in medium composition can expand the proliferative potential of human mammary epithelial cells (HMEC) initiated as primary cultures to 50 to 60 population doublings followed by p16-positive, senescence-associated beta-galactosidase-positive stasis. We compared the properties of growing and senescent pre-stasis HMEC with growing and senescent post-selection HMEC, that is, cells grown in a serum-free medium that overcame stasis via silencing of p16 expression and that display senescence associated with telomere dysfunction. Cultured pre-stasis populations contained cells expressing markers associated with luminal and myoepithelial HMEC lineages in vivo in contrast to the basal-like phenotype of the post-selection HMEC. Gene transcript and protein expression, DNA damage-associated markers, mean telomere restriction fragment length, and genomic stability differed significantly between HMEC populations at the stasis versus telomere dysfunction senescence barriers. Senescent isogenic fibroblasts showed greater similarity to HMEC at stasis than at telomere dysfunction, although their gene transcript profile was distinct from HMEC at both senescence barriers. These studies support our model of the senescence barriers encountered by cultured HMEC in which the first barrier, stasis, is retinoblastoma-mediated and independent of telomere length, whereas a second barrier (agonescence or crisis) results from telomere attrition leading to telomere dysfunction. Additionally, the ability to maintain long-term growth of genomically stable multilineage pre-stasis HMEC populations can greatly enhance experimentation with normal HMEC.
培养的正常人类上皮细胞通常显示出有限的增殖潜能,在遇到与细胞周期蛋白依赖性激酶抑制剂p16和/或p21水平升高相关的应激相关衰老屏障(停滞)之前,大约有10到40次群体倍增。我们现在表明,培养基成分的简单变化可以将作为原代培养起始的人乳腺上皮细胞(HMEC)的增殖潜能扩展到50到60次群体倍增,随后是p16阳性、衰老相关β-半乳糖苷酶阳性的停滞。我们比较了处于生长和衰老前期停滞状态的HMEC与经过筛选后处于生长和衰老状态的HMEC的特性,即那些在无血清培养基中生长、通过p16表达沉默克服停滞且表现出与端粒功能障碍相关衰老的细胞。与筛选后HMEC的基底样表型相反,培养的前期停滞群体包含表达与体内管腔和肌上皮HMEC谱系相关标志物的细胞。在停滞与端粒功能障碍衰老屏障时,HMEC群体之间的基因转录本和蛋白质表达、DNA损伤相关标志物、平均端粒限制片段长度以及基因组稳定性存在显著差异。衰老的同基因成纤维细胞在停滞时与HMEC的相似性高于在端粒功能障碍时,尽管它们在两个衰老屏障时的基因转录本谱都与HMEC不同。这些研究支持了我们关于培养的HMEC所遇到的衰老屏障的模型,其中第一个屏障,即停滞,是由视网膜母细胞瘤介导的且与端粒长度无关,而第二个屏障(衰老或危机)是由端粒磨损导致端粒功能障碍引起的。此外,维持基因组稳定的多谱系前期停滞HMEC群体长期生长的能力可以极大地增强对正常HMEC的实验。