1. ¹Department of Reproductive Medicine and Surgery, Faculty of Medical and Pharmaceutical Science, Kumamoto University, Honjo 1-1-1, Kumamoto-City, Kumamoto 860-8556, Japan
2. ²Department of Gynecology, Faculty of Medical and Pharmaceutical Science, Kumamoto University, Honjo 1-1-1, Kumamoto-City, Kumamoto 860-8556, Japan
3. ³Virology Devision, National Cancer Center Research Institute, 5-1-1 Tsukiji, Chuo-ku, Tokyo 104-0045, Japan

Correspondence: Professor H Katabuchi, E-mail: buchi@kaiju.medic.kumamoto-u.ac.jp

Received 27 January 2005; Revised 26 April 2005; Accepted 18 May 2005; Published online 14 June 2005.

Abstract

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 (E6151), and Bmi1 polycomb gene, in combination with telomerase reverse transcriptase (hTERT). Consequently, five HOSE1s cell lines, HOSE1s-E6/hTERT, -E7/hTERT, -E6/E7/hTERT, -E6151/E7/hTERT, and -E6151/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.