Hietanen S, Syrjänen K, Syrjänen S
Department of Obstetrics and Gynecology, Turku University Hospital, Finland.
Br J Cancer. 1998 Mar;77(5):766-75. doi: 10.1038/bjc.1998.125.
Two cell lines derived from vaginal intraepithelial neoplasias (VAINs) expressing human papillomavirus (HPV) 33 (VAIN I, UT-DEC-1) and 16 (VAIN II, UT-DEC-2) E6-E7 mRNA were studied in organotypic culture for their keratins and cell cycle regulatory proteins in relation to replicative aging. Early-passage UT-DEC-1 and UT-DEC-2 cells reproduced epithelial patterns consistent with VAIN. Cells from later passages resembled full-thickness intraepithelial neoplasia (UT-DEC-1) and microinvasive cancer (UT-DEC-2). The morphological changes were compatible with these cell lines' ability for anchorage-independent growth at later passages. Simple epithelial keratins were aberrantly expressed in both cell lines. K18 (absent in normal vaginal keratinocytes) and K17 expression increased in UT-DEC-1 and UT-DEC-2 cells at late passages. No marked differences in expression of p53 (wild type in both cell lines), mdm-2 or PCNA were detected in parallel with progression. The expression of p21WAF1/cip1 localized mostly to the upper half of the epithelium at early passage and was more intense in the HPV 16-positive UT-DEC-2 cell line expressing K10. In Northern blot analyses, the transcription pattern of the HPV 33 E6-E7 of the UT-DEC-1 cell line changed during later passages, whereas that of the HPV 16 E6-E7 of the UT-DEC-2 cell line remained unaltered. The present characterization of the phenotype of these cell lines derived from natural squamous intraepithelial lesions shows an association between simple epithelial-type keratin expression and progressive changes in growth and morphology, but fails to demonstrate consistent changes in the expression of cell cycle regulatory proteins studied in parallel with progression.
对源自表达人乳头瘤病毒(HPV)33(VAIN I,UT-DEC-1)和16(VAIN II,UT-DEC-2)E6-E7信使核糖核酸的阴道上皮内瘤变(VAINs)的两种细胞系进行了器官型培养研究,以观察其角蛋白和细胞周期调节蛋白与复制性衰老的关系。早期传代的UT-DEC-1和UT-DEC-2细胞重现了与VAIN一致的上皮模式。后期传代的细胞类似于全层上皮内瘤变(UT-DEC-1)和微浸润癌(UT-DEC-2)。形态学变化与这些细胞系在后期传代时的非锚定依赖性生长能力相符。两种细胞系中均异常表达了简单上皮角蛋白。晚期传代时,UT-DEC-1和UT-DEC-2细胞中K18(正常阴道角质形成细胞中不存在)和K17表达增加。随着进程推进,未检测到p53(两种细胞系中均为野生型)、mdm-2或增殖细胞核抗原表达的明显差异。p21WAF1/cip1的表达在早期传代时主要定位于上皮的上半部分,在表达K10的HPV 16阳性UT-DEC-2细胞系中更为强烈。在Northern印迹分析中,UT-DEC-1细胞系的HPV 33 E6-E7转录模式在后期传代时发生了变化,而UT-DEC-2细胞系的HPV 16 E6-E7转录模式保持不变。这些源自自然鳞状上皮内病变的细胞系的表型特征表明,简单上皮型角蛋白表达与生长和形态的渐进性变化之间存在关联,但未能证明与进程平行研究的细胞周期调节蛋白表达存在一致变化。