Expression of activated PIK3CA in ovarian surface epithelium results in hyperplasia but not tumor formation.

Détails

ID Serval
serval:BIB_81B92DEAD82F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Expression of activated PIK3CA in ovarian surface epithelium results in hyperplasia but not tumor formation.
Périodique
Plos One
Auteur(s)
Liang S., Yang N., Pan Y., Deng S., Lin X., Yang X., Katsaros D., Roby K.F., Hamilton T.C., Connolly D.C., Coukos G., Zhang L.
ISSN
1932-6203 (Electronic)
ISSN-L
1932-6203
Statut éditorial
Publié
Date de publication
2009
Volume
4
Numéro
1
Pages
e4295
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov'tPublication Status: ppublish
Résumé
BACKGROUND: The Phosphatidylinositol 3'-kinase is a key regulator in various cancer-associated signal transduction pathways. Genetic alterations of its catalytic subunit alpha, PIK3CA, have been identified in ovarian cancer. Our in vivo data suggests that PIK3CA activation is one of the early genetic events in ovarian cancer. However, its role in malignant transformation of ovarian surface epithelium (OSE) is largely unclear.
METHODOLOGY/PRINCIPAL FINDINGS: Using the Müllerian inhibiting substance type II receptor (MISIIR) promoter, we generated transgenic mice that expressed activated PIK3CA in the Müllerian epithelium. Overexpression of PIK3CA in OSE induced remarkable hyperplasia, but was not able to malignantly transform OSE in vivo. The consistent result was also observed in primary cultured OSEs. Although enforced expression of PIK3CA could not induce OSE anchorage-independent growth, it significantly increased anchorage-independent growth of OSE transformed by mutant K-ras.
CONCLUSIONS/SIGNIFICANCE: While PIK3CA activation may not be able to initiate OSE transformation, we conclude that activation of PIK3CA may be an important molecular event contributing to the maintenance of OSE transformation initiated by oncogenes such as K-ras.
Mots-clé
Animals, Cell Line, Tumor, Enzyme Activation, Epithelium/enzymology, Female, Gene Expression Regulation, Enzymologic, Gene Expression Regulation, Neoplastic, Genes, ras, Humans, Hyperplasia, Mice, Mice, Transgenic, Ovary/enzymology, Phosphatidylinositol 3-Kinases/biosynthesis, Phosphatidylinositol 3-Kinases/genetics
Pubmed
Open Access
Oui
Création de la notice
14/10/2014 12:43
Dernière modification de la notice
08/05/2019 21:10
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