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Establishment of an immortalised human ovarian surface epithelial cell line without chromosomal instability.

Maeda T, Tashiro H, Katabuchi H, Begum M, Ohtake H, Kiyono T, Okamura H - Br. J. Cancer (2005)

Bottom Line: Our goal was to establish new immortalised human OSE cells that retain the original characteristics of the primary cells without chromosomal alterations.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Reproductive Medicine and Surgery, Faculty of Medical and Pharmaceutical Science, Kumamoto University, Honjo 1-1-1, Kumamoto-City, Kumamoto 860-8556, Japan.

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 (E6delta151), and Bmi1 polycomb gene, in combination with telomerase reverse transcriptase (hTERT). Consequently, five HOSE1s cell lines, HOSE1s-E6/hTERT, -E7/hTERT, -E6/E7/hTERT, -E6delta151/E7/hTERT, and -E6delta151/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.

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Karyotype of HOSE1-E7/hTERT cells. The chromosomal number was diploid after long–term culture (passage number 41; population doubling 142).
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fig3: Karyotype of HOSE1-E7/hTERT cells. The chromosomal number was diploid after long–term culture (passage number 41; population doubling 142).

Mentions: Although HOSE1s-E6/hTERT, -E6/E7/hTERT, -E6Δ151/E7/hTERT, and -E6Δ151/Bmi1/hTERT exhibited almost normal chromosomal number with small deviation ranging between 42 and 48 in early passage (passage 16), they did show chromosomal alteration varying from 43 to 96 after immortalisation (passage 41) (Table 2A). HOSE1-E7/hTERT alone revealed normal diploidy in both passages (Figure 3 and Table 2B). In late passage (passage 41), the G-banded karyotype of this cell line was normal in five of 12 cells, 46, XX, showed minor structural alteration including 46, XX, t(7;7)(p10;p10) in five of 12 cells, and showed 46, idem, -X, +i(X)(p10), add(1)(p36), add(10)(p11) in two of 12 cells (Table 2B). Futhermore, karyotype of the HOSE1-E7/hTERT cells at passage 60 was additionally analysed. All 50 cells revealed also diploidy and the G-banded karyotype of this was 46, XX in three of 13 cells and showed a minor structural alteration indicated 46, XX, t(7;7)(p10;p10) in 10 of 13 cells.


Establishment of an immortalised human ovarian surface epithelial cell line without chromosomal instability.

Maeda T, Tashiro H, Katabuchi H, Begum M, Ohtake H, Kiyono T, Okamura H - Br. J. Cancer (2005)

Karyotype of HOSE1-E7/hTERT cells. The chromosomal number was diploid after long–term culture (passage number 41; population doubling 142).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2361470&req=5

fig3: Karyotype of HOSE1-E7/hTERT cells. The chromosomal number was diploid after long–term culture (passage number 41; population doubling 142).
Mentions: Although HOSE1s-E6/hTERT, -E6/E7/hTERT, -E6Δ151/E7/hTERT, and -E6Δ151/Bmi1/hTERT exhibited almost normal chromosomal number with small deviation ranging between 42 and 48 in early passage (passage 16), they did show chromosomal alteration varying from 43 to 96 after immortalisation (passage 41) (Table 2A). HOSE1-E7/hTERT alone revealed normal diploidy in both passages (Figure 3 and Table 2B). In late passage (passage 41), the G-banded karyotype of this cell line was normal in five of 12 cells, 46, XX, showed minor structural alteration including 46, XX, t(7;7)(p10;p10) in five of 12 cells, and showed 46, idem, -X, +i(X)(p10), add(1)(p36), add(10)(p11) in two of 12 cells (Table 2B). Futhermore, karyotype of the HOSE1-E7/hTERT cells at passage 60 was additionally analysed. All 50 cells revealed also diploidy and the G-banded karyotype of this was 46, XX in three of 13 cells and showed a minor structural alteration indicated 46, XX, t(7;7)(p10;p10) in 10 of 13 cells.

Bottom Line: Our goal was to establish new immortalised human OSE cells that retain the original characteristics of the primary cells without chromosomal alterations.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Reproductive Medicine and Surgery, Faculty of Medical and Pharmaceutical Science, Kumamoto University, Honjo 1-1-1, Kumamoto-City, Kumamoto 860-8556, Japan.

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 (E6delta151), and Bmi1 polycomb gene, in combination with telomerase reverse transcriptase (hTERT). Consequently, five HOSE1s cell lines, HOSE1s-E6/hTERT, -E7/hTERT, -E6/E7/hTERT, -E6delta151/E7/hTERT, and -E6delta151/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.

Show MeSH
Related in: MedlinePlus