Edith BONNELYE PhD Cellular Biology

Course and current status

Since May 2021           DR2 CNRS - Institut de Biologie de Lille- dans l’équipe Target, du Dr D TULASNE -dans l’Unité UMR 9020 CNRS - UMR-S 1277 Inserm dirigée par le Dr Isabelle VANSEUNINGEN -Lille

2019 - 2021                 CRCN CNRS Institut cancérologie de l'Ouest INSERM U1232, Team of Dr François VALLETTE, CRCINA (Nantes). Since october 2021. Director of Research class 2, CNRS 

12th November 2013         HDR University Lyon I

2006-2019                     CRCN CNRS Physiopathology, Diagnostic and Treatments of bone diseases INSERM, UMR1033 Faculty of Medicine Laennec. Directed by Dr Philippe Clézardin. Lyon, France

2002 - 2006                  CR2 CNRS department of molecular and cellular biology, UMR 5161 CNRS /ENS directed by E Gilson., Lyon, France (Dr Pierre JURDIC lab)

1998 - 2002                  Post doctoral training, department of Anatomy and cellular biology laboratory directed by Dr Jane Aubin, University of Toronto, Canada.

1994 - 1997                  PhD (U.S.T.L. Lille) In molecular oncology Unit, CNRS URA1160, directed by Pr Dominique Stéhelin. Lille, France

Scientific summary

Bone metastases are one of the main complications of breast and prostate cancer. Indeed, up to 70 percent of patients with advanced breast cancer (BCa) and 80 percent of patients dying from prostate cancer (PCa) have developed bone metastases that are incurable, raising the need to improve their treatment and prevention. We identified the nuclear receptor ERRa (“Estrogen Related Receptor alpha”) in bone physiology in osteoblasts and osteoclasts and as an actor in bone metastases progression from breast and prostate cancer. First, we described ERRa as an inhibitor in BCa bone metastases by acting as an immunity modulator through the regulation of chemokines (CCL17, CCL20) and the TGFb signaling allowing CD8+ T Lymphocytes recruitment and cytotoxic features. Second, we identified ERRa as a pro-metastatic factor in PCa by associating ERRa to the lethal castration resistant prostate cancer (CRPC) stage. Moreover, in PCa, we described ERRa as a pro-bone metastatic factor by impacting the bone remodelling and the tumor infiltrating fibroblasts (CAF) through the regulation of VEGFa, TGFb and WNT signaling in tumor cells and periostin in CAF. In conclusion, this new knowledge on ERRa suggest a dual role of this receptor in bone metastases from BCa and PCa. There also show that ERRa may constitute a new aggressiveness biomarker associated with high risk of CRPC progression and suggest that targeting ERRa in PCa may constitute a new therapeutic strategy in the treatment of the CRPC and their associated bone metastases.

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