Email updates

Keep up to date with the latest news and content from Molecular Cancer and BioMed Central.

Open Access Highly Accessed Research

An essential role for Ran GTPase in epithelial ovarian cancer cell survival

Véronique Barrès1, Véronique Ouellet1, Julie Lafontaine1, Patricia N Tonin234, Diane M Provencher156 and Anne-Marie Mes-Masson16*

Author Affiliations

1 Centre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM)/Institut du cancer de Montréal,1560 Sherbrooke Est, Montreal, H2L 4M1, Canada

2 Department of Medicine, McGill University, Montreal, Canada

3 Department of Human Genetics, McGill University, Montreal, Canada

4 Research Institute of McGill University Health Centre (RI-MUHC), 1650 Cedar Avenue, Montreal, H3G 1A4, Quebec, Canada

5 Department of Obstetric-Gynecology/Université de Montréal, Montreal, Canada

6 Départment of Medecine, Université de Montréal, Montreal, Canada

For all author emails, please log on.

Molecular Cancer 2010, 9:272  doi:10.1186/1476-4598-9-272

Published: 13 October 2010

Abstract

Background

We previously identified that Ran protein, a member of the Ras GTPase family, is highly expressed in high grade and high stage serous epithelial ovarian cancers, and that its overexpression is associated with a poor prognosis. Ran is known to contribute to both nucleocytoplasmic transport and cell cycle progression, but its role in ovarian cancer is not well defined.

Results

Using a lentivirus-based tetracycline-inducible shRNA approach, we show that downregulation of Ran expression in aggressive ovarian cancer cell lines affects cellular proliferation by inducing a caspase-3 associated apoptosis. Using a xenograft tumor assay, we demonstrate that depletion of Ran results in decreased tumorigenesis, and eventual tumor formation is associated with tumor cells that express Ran protein.

Conclusion

Our results suggest a role for Ran in ovarian cancer cell survival and tumorigenicity and suggest that this critical GTPase may be suitable as a therapeutic target.