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角质形成细胞特异性POU转录因子hSkn-1a抑制宫颈癌细胞系的生长。

Keratinocyte-specific POU transcription factor hSkn-1a represses the growth of cervical cancer cell lines.

作者信息

Enomoto Yutaka, Enomoto Kikuko, Kitamura Tadaichi, Kanda Tadahito

机构信息

1Division of Molecular Genetics, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku-ku, Tokyo 162-8640, Japan.

出版信息

Oncogene. 2004 Jun 24;23(29):5014-22. doi: 10.1038/sj.onc.1207653.

Abstract

The POU transcription factor human Skn-1a (hSkn-1a) specifically promotes the proliferation of keratinocytes and enhances their differentiation. We examined the effects of hSkn-1a on cervical cancer cell lines of epithelial origin, in which the differentiation program is interrupted. From HeLa/Tet-On, a clone that can be induced to make hSkn-1a by doxycycline (HeLa/hSkn-1a) was prepared and characterized. Shortly after the induction, the cells expressed cytokeratin 10 (K10), a major marker protein in differentiating keratinocytes. While maintained for several days in the presence of doxycycline, the HeLa/hSkn-1a cells showed a slightly prolonged time of population doubling, the occasional appearance of flat cells with lowered DNA synthesis, and a low level of apoptotic DNA fragmentation. In SiHa and HeLa S3 cultures, K10 mRNA and apoptotic DNA fragmentation were detected at 48 h after infection with an adenoviral vector capable of expressing hSkn-1a. A colony inhibition assay showed that the growth of HeLa S3, SiHa, CaSki, and C-33A cells was repressed, as seen from the decreased number and average size of the drug-resistant colonies at 2 or 3 weeks after transfection with a plasmid that can express hSkn-1a and neomycin resistance gene. These results suggest that the expression of hSkn-1a represses the growth of the cervical cancer cells through the partial resumption of the differentiation pathway followed by slow suppression of cell replication and apoptosis.

摘要

POU转录因子人类Skn-1a(hSkn-1a)可特异性促进角质形成细胞的增殖并增强其分化。我们研究了hSkn-1a对上皮来源的宫颈癌细胞系的影响,这些细胞系的分化程序被中断。从HeLa/Tet-On细胞系中制备并鉴定了一个可通过强力霉素诱导产生hSkn-1a的克隆(HeLa/hSkn-1a)。诱导后不久,细胞表达细胞角蛋白10(K10),这是分化的角质形成细胞中的一种主要标记蛋白。在强力霉素存在的情况下维持培养数天后,HeLa/hSkn-1a细胞的群体倍增时间略有延长,偶尔会出现DNA合成降低的扁平细胞,且凋亡DNA片段化水平较低。在SiHa和HeLa S3培养物中,用能够表达hSkn-1a的腺病毒载体感染48小时后,检测到K10 mRNA和凋亡DNA片段化。集落抑制试验表明,用能够表达hSkn-1a和新霉素抗性基因的质粒转染2或3周后,HeLa S3、SiHa、CaSki和C-33A细胞的生长受到抑制,从耐药集落的数量减少和平均大小减小可以看出。这些结果表明,hSkn-1a的表达通过部分恢复分化途径,随后缓慢抑制细胞复制和凋亡来抑制宫颈癌细胞的生长。

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