Céline Guigon
  • E-mail :[email]
  • Phone : +33157278404
  • Location : Paris, France
Last update 2019-02-06 10:13:48.275

Céline Guigon PhD Cell Signaling, Endocrinology & Reproductive Biology

Course and current status

Current position:

Research Associate; CR1 Inserm U1133, University Paris 7, CNRS-EAC4413, Paris, France.

Education:

2000-2004    PhD Cell Signaling, Endocrinology & Reproductive Biology, University Paris11, Le Kremlin-Bicêtre, France.

1999-2000    Master in Physiology of Reproduction, University Paris 6, Paris, France.

1998-1999   Bachelor in Cellular Biology and Physiology, University Paris 6, Paris, France.

 

Chronology of Employment:

Jan-Sept 2005:  Postdoctoral Fellow, Laboratory of Physiology and Physiopathology, University Paris 6, Paris, France.

2005-2010: Postdoctoral Fellow, Gene Regulation Section, Laboratory of Molecular Biology, Center for Cancer Research, National Cancer Institute, National Institutes of Health

Nov 2010-Oct 2011: Postdoctoral Fellow, Physiology of Gonadotropic Axis Group, Unit of Functional and Adaptive Biology, University Paris Diderot-Paris, France.

 

Honors and Other Special Scientific Recognition: 

2010-Fondation pour la Recherche Medicale (FRM) postdoctoral fellowship

2008-Exceptional Stipend Increase

2008-NIH FARE 2009 award 

2007-Annual Meeting of the Endocrine Society Travel Award. 

2003-Cancer Association Research (ARC) Doctoral Fellowship.

2002-Annual Meeting of the French Society of Endocrinology (SFE) Travel Fellowship.

2002-American Society for the Study of Reproduction (SSR) Travel Fellowship.

2000-French Ministery of Research Doctoral Fellowship.

Scientific summary

Researches in my group focus on the regulation of ovarian activity in both physiological and pathological conditions.

 They are centered on two main axis:

  1- Implication of Estradiol Signaling in Ovarian Granulosa Cell Tumors

Estradiol (E2) is mainly produced by the ovary and plays a crucial role in fertility by regulating the different components of the gonadotropic axis during the sexual cycle. In the ovary, it is essential for the growth of ovarian follicles until ovulation. This hormone acts via nuclear receptors (ERα and ERβ) or through a receptor coupled to a G protein (GPER, G protein-coupled estrogen receptor). Whether deregulation of estradiol signaling can occur in granulosa cell tumors is unknown. This pathology remains difficult to treat because recurrences occur even when the tumor is detected at an early stage. Despite the crucial role of this hormone in the ovary, its mechanisms of action remain paradoxically poorly known during the tumor process. Our team is interested in the roles and mechanisms of action of E2 in this pathology. Our approaches are based on molecular and cellular tools with tumor cell lines and human primary cultures, as well as on mouse models of the disease (tumor cell xenografts, transgenic mice) and on biopsies obtained in collaboration with hospital services (Drs Leary & Génestie, Institut Gustave Roussy, Villejuif; Drs Treilleux & Cocquard, Léon Bérard Center, Lyon, Prs Grynberg & Friedman, Béclère Hospital, Clamart). We have already demonstrated in vitro the inhibitory effect of GPER in the migration of metastatic granulosa cells (François et al, Carcinogenesis 2015). We are now evaluating the contribution of nuclear E2 receptors and their modes of genomic and non-genomic action, in collaboration with Pr. Katzenellenbogen (Illinois University). Deciphering the mechanisms of action of E2 in this disease should help in developing novel therapeutic approaches for targeting the receptor (s) involved. (Grants: Marie Curie reintegration grant Funding, Ligue contre le cancer Ile-de-France, Subvention ARC, GEFLUC).


2-Mechanisms involved in the activation of the ovary during mini-puberty

The ovary produces significant amounts of E2 just after birth in mammals, a period otherwise known as "mini-puberty of childhood". This production of E2, although transitory, seems to play a crucial role in fertility programming, especially for the implementation of puberty. However, the mechanisms involved in the regulation of the infant ovary are not well known. It is in this context we have developed a research program aimed at understanding the physiological activation of the infant ovary. We mainly use in vivo approaches on the murine model, in situ approaches on the human infant ovary (Collab, Pr Ravel, Inserm U1085, IRSET, Rennes South Hospital) and in vitro studies on granulosa cell lines and primary cultures (Collab. Prs Grynberg & Friedman, Béclère Hospital, Clamart). Our work has shown that the marked rise in pituitary hormones FSH and LH in the infant period is responsible for the high production of E2 by follicles in ovarian growth (François et al, Scientific Report, 2017). We have recently shown that this results from the inhibition by FSH of the expression of antimüllerian hormone (AMH) in these growing follicles (Devillers et al, J Endocr 2019). We are now analyzing the molecular mechanisms of action of pituitary hormones on the infant ovary to understand how they can stimulate E2 production without impacting follicular growth, unlike what happens in the cyclic ovary. Another field of investigation of our group is to determine whether the signaling of the aryl hydrocarbon receptor (AHR, dioxin receptor) can influence the early functioning of the ovary (Collab Pr Coumoul, University Paris 5).

This work has been supported by grants from the Research Executive Agency of the European Commission (Marie Curie Reintegration grant, ESTROVARYTUMOUR # 276970), by La Ligue Contre Le Cancer, by La Fondation Pour la Recherche Médicale (FRM, programme espoir de la recherche), by ARC (Subvention ARC) and by GEFLUC. 

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