Amplification of R-spondin1 signaling induces granulosa cell fate defects and cancers in mouse adult ovary View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-01

AUTHORS

M-C De Cian, E Pauper, R Bandiera, V P I Vidal, S Sacco, E P Gregoire, A-A Chassot, C Panzolini, D Wilhelm, E Pailhoux, S A Youssef, A de Bruin, K Teerds, A Schedl, I Gillot, M-C Chaboissier

ABSTRACT

R-spondin1 is a secreted regulator of WNT signaling, involved in both embryonic development and homeostasis of adult organs. It can have a dual role, acting either as a mitogen or as a tumor suppressor. During ovarian development, Rspo1 is a key factor required for sex determination and differentiation of the follicular cell progenitors, but is downregulated after birth. In human, increased RSPO1 expression is associated with ovarian carcinomas, but it is not clear whether it is a cause or a consequence of the tumorigenic process. To address the role of Rspo1 expression in adult ovaries, we generated an Rspo1 gain-of-function mouse model. Females were hypofertile and exhibited various ovarian defects, ranging from cysts to ovarian tumors. Detailed phenotypical characterization showed anomalies in the ovulation process. Although follicles responded to initial follicle-stimulating hormone stimulation and developed normally until the pre-ovulatory stage, they did not progress any further. Although non-ovulated oocytes degenerated, the surrounding follicular cells did not begin atresia. RSPO1-induced expression not only promotes canonical WNT signaling but also alters granulosa cell fate decisions by maintaining epithelial-like traits in these cells. This prevents follicle cells from undergoing apoptosis, leading to the accumulation of granulosa cell tumors that reactivates the epithelial program from their progenitors. Taken together, our data demonstrate that activation of RSPO1 is sufficient in promoting ovarian tumors and thus supports a direct involvement of this gene in the commencement of ovarian cancers. More... »

PAGES

208-218

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/onc.2016.191

DOI

http://dx.doi.org/10.1038/onc.2016.191

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051515681

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27270435


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