Establishment of an immortalised human ovarian surface epithelial cell line without chromosomal instability
Establishment of an immortalised human ovarian surface epithelial cell line without chromosomal instability
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DOI：
10.1038/sj.bjc.6602662
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发表时间：
2005-07-11
影响因子：
8.8
通讯作者：
Okamura, H
中科院分区：
文献类型：
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作者：
Maeda, T;Tashiro, H;Okamura, H
卵巢上皮癌被认为源自卵巢表面上皮（OSE）。使用永生化人类 OSE 细胞的实验系统的开发正在解释卵巢癌发生的早期分子变化的黑匣子。然而，由于染色体不稳定，现有的 OSE 细胞系的实用性有限。我们的目标是建立新的永生化人类 OSE 细胞，保留原代细胞的原始特征，而不发生染色体改变。使用从患有子宫内膜癌的绝经后患者获得的原代人OSE细胞，通过用含有16型人乳头瘤病毒（HPV-16）E6、E7、变种E6（E6D151）和Bmi1多梳基因的逆转录病毒表达载体感染，并结合端粒酶逆转录酶，新建立了5种细胞系（“HOSE1”系）。 hTERT）。因此，五个 HOSE1s 细胞系，HOSE1s-E6/hTERT、-E7/hTERT、-E6/E7/hTERT、-E6D151/E7/hTERT 和 -E6D151/Bmi1/hTERT，生长超过了 200 个群体倍增数。除了 HOSE1-E6/hTERT 之外，这些细胞系基本上显示了原代人 OSE 细胞的原始特征。其中，HOSE1-E7/hTERT 在核型分析中保留了二倍体，并且在不依赖贴壁的生长和肿瘤形成中没有显示出转化的表型。因此，HOSE1-E7/hTERT 可能提供一个新的模型系统来研究早期分子变化的机制。
Epithelial ovarian carcinoma is thought to derive from ovarian surface epithelium (OSE). The black box of the early molecular changes in ovarian carcinogenesis is being interpreted by the development of experimental systems employing immortalised human OSE cells. However, the existing cell lines of the OSE cells have limited utility due to chromosomal instability. Our goal was to establish new immortalised human OSE cells that retain the original characteristics of the primary cells without chromosomal alterations. Using primary human OSE cells obtained from a postmenopausal patient with endometrial cancer, five cell lines ('HOSE1' lines) were newly established by infection with retroviral expression vectors containing type 16 human papillomavirus (HPV-16) E6, E7, a variant E6 (E6D151), and Bmi1 polycomb gene, in combination with telomerase reverse transcriptase ( hTERT). Consequently, five HOSE1s cell lines, HOSE1s- E6/hTERT, - E7/hTERT, - E6/E7/hTERT, - E6D151/E7/hTERT, and - E6D151/Bmi1/ hTERT, grew beyond the population doubling number of 200. These cell lines, except for HOSE1-E6/hTERT, essentially showed the original features of the primary human OSE cells. Of them, HOSE1-E7/hTERT preserved diploidy in a kariotype analysis, and did not show transformed phenotypes in anchorage-independent growth and tumour formation. Thus, HOSE1-E7/hTERT may provide a novel model system with which to investigate the mechanisms of early molecular changes.