| First Author | Usongo M | Year | 2013 |
| Journal | Dev Dyn | Volume | 242 |
| Issue | 3 | Pages | 291-300 |
| PubMed ID | 23239518 | Mgi Jnum | J:193046 |
| Mgi Id | MGI:5467459 | Doi | 10.1002/dvdy.23919 |
| Citation | Usongo M, et al. (2013) Activation of the Canonical WNT Signaling Pathway Promotes Ovarian Surface Epithelial Proliferation Without Inducing beta-Catenin/Tcf-Mediated Reporter Expression. Dev Dyn 242(3):291-300 |
| abstractText | Background: In response to activation of the canonical WNT signaling pathway, beta-catenin cooperates with Lef/Tcf (lymphoid enhancer factor/T-cell factor) transcription factors to drive expression of Wnt target genes. The canonical WNT signaling pathway is involved in development, wound repair, and tumorigenesis. Studies examining the involvement of the canonical WNT signaling pathway in the development of ovarian surface epithelium (OSE) and ovarian carcinogenesis, however, have recently begun to emerge. In this study, we investigated the modulation of beta-catenin and beta-catenin/Tcf-signaling activity within the OSE using responsive transgenic mice and examined the response of primary OSE cells and ovarian cancer cell lines to activation of the canonical WNT signaling pathway. Results: beta-catenin was localized to the lateral membrane of the ovarian epithelium. Stimulation of primary OSE cells in vitro with LiCl or Wnt3a led to GSK-3beta inhibition and stabilization of beta-catenin but failed to induce beta-catenin/Tcf-mediated lacZ expression. Furthermore, E-cadherin expression was downregulated and the proliferative potency of OSE cells increased. Of four ovarian cancers cell lines screened, only the HEY cell line demonstrated induction of luciferase reporter upon canonical WNT stimulation. Conclusions: These observations suggest that in ovarian adenocarcinoma, dysregulated WNT signaling may not always be indicative of beta-catenin/Tcf-mediated transcriptional activity. Developmental Dynamics 242:291-300, 2013. (c) 2012 Wiley Periodicals, Inc. |
