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Updated: Aug 11, 2026

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression
12:42

Heterotypic Three-dimensional In Vitro Modeling of Stromal-Epithelial Interactions During Ovarian Cancer Initiation and Progression

Published on: August 28, 2012

C-erbB-2 or mutant Ha-ras induced malignant transformation of immortalized human ovarian surface epithelial cells in

T Kusakari1, M Kariya, M Mandai

  • 1Department of Gynecology and Obstetrics, Faculty of Medicine, Kyoto University, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606-5807, Japan.

British Journal of Cancer
|December 17, 2003
PubMed

Insights

This study investigated ovarian cancer development. Introducing specific genes (c-erbB-2 or mutant Ha-ras) into ovarian surface cells induced tumor formation, suggesting their role in ovarian carcinogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Ovarian cancer is thought to arise from ovarian surface epithelium due to accumulating gene abnormalities.
  • The precise role of these genetic aberrations in ovarian carcinogenesis remains unclear.

Purpose of the Study:

  • To investigate the involvement of specific genes in ovarian carcinogenesis.
  • To elucidate the process by which gene abnormalities contribute to ovarian cancer development.

Main Methods:

  • Genes frequently altered in human ovarian cancers were transfected into human ovarian surface epithelial cells.
  • Cells were immortalized using SV40 large T antigen (LT) and human telomerase reverse transcriptase (hTERT).
  • Subsequent transfection with c-erbB-2 or mutant Ha-ras genes was performed, followed by tumorigenesis assays in mice.

Main Results:

  • Immortalized cells alone did not form tumors.
  • Transfection with c-erbB-2 or mutant Ha-ras induced anchorage-independent growth and tumorigenesis in mice (50% and 40% incidence, respectively).
  • Tumorigenic cells showed increased vascular endothelial growth factor secretion under hypoxia and enhanced apoptosis resistance.

Conclusions:

  • The introduction of c-erbB-2 or mutant Ha-ras into immortalized ovarian surface epithelial cells can induce tumorigenicity.
  • These findings suggest that c-erbB-2 and mutant Ha-ras genes may play a significant role in ovarian carcinogenesis.

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