Vincent Goffin was trained as a molecular endocrinologist. He graduated at the University of Liège (Belgium) in 1993. After his post-doctoral training at Inserm U344, Paris (Marie-Curie fellowship), he was hired by Inserm as a tenure researcher in 1996. He is currently Research Director and heads his lab since 2006. Vincent Goffin is internationally recognized as a leader in the field of the prolactin (PRL)/growth hormone (GH) protein family. His main achievements include i) translational research on the role of PRL receptor signaling in various human diseases, with particular emphasis in Oncology, ii) preclinical development of PRL receptor inhibitors (used worldwide in academic labs) based on cutting-edge structure-function studies of receptor activation. In 2012, he founded the FASEB Science Research Conference “The GH/PRL family in biology & diseases” (ongoing conference in the FASEB series). He is/has been consultant for several companies developing PRL-related compounds and Editorial Board member or Associate Editor of 9 peer-review Journals in the field of onco-endocrinology. More recently, his research focused on prostate pathophysiology leading to the discovery in mouse models of castration-resistant luminal progenitors potentially involved in both benign prostatic hyperplasia etiology and prostate cancer relapse.

Focus

Use translational approaches to identify, understand and target cellular and molecular mechanisms responsible for the progression and resistance to treatment of prostate and breast tumors (benign and cancer), with major emphasis on prolactin, calcium, iron and stem cells.

Introduction

Breast cancer is the most commonly occurring cancer in women, and prostate cancer the second most common cancer in men. Due to the increasing lifespan in western countries, cancer incidence will continue to raise in future. When diagnosed at a localized stage, breast and prostate cancers are successfully treated by focal intervention (surgery, radiotherapy), which supports routine prevention policies (e.g. PSA screening, mammography). The standard of care of more advanced stages of the diseases involves medical treatment (e.g. anti-androgen therapy, chemotherapy). Although some tumors respond well to therapy, de novo or acquired resistance to treatment is frequently observed, leading to cancer progression towards lethal metastatic stages.

Although benign breast and prostate tumors do not predispose to cancer, they alter the quality of life of patients, e.g. lower urinary tract symptoms for patients presenting with benign prostatic hyperplasia. Beyond surgery, medical treatment of benign tumors are often empirical (breast) or face exhaustion of effect (prostate).

To improve treatment efficacy, new therapies need to be developed, which requires i) to identify the cells that resist to treatment and drive tumor relapse, ii) to better understand the mechanisms they use in escape treatment, and iii) to identify new actionable targets. Our studies mainly focus on prolactin and calcium pathways, iron metabolism, oxidative stress, inflammation and stem cell biology. Our translational approach involves the use of cell lines, primary cultures (human, mouse), genetically-modified mouse models and patient samples.

Research objectives

1. Characterize castration-tolerant prostate cell(s) by single cell transcriptomics and identify new actionable targets to prevent prostate cancer relapse (PIs: Dr Vincent GOFFIN and Dr Jacques-Emmanuel GUIDOTTI)
2. Use in vitro models of benign prostate hyperplasia and prostate cancer to investigate the effects of drug treatments on neuroendocrine differentiation / Isolation of prostate tumoral cells from liquid biopsies (PIs: Dr Thierry CAPIOD and Pr PATERLINI-BRECHOT)
3. Study of iron metabolism and ferroptosis in breast cancer stem cells and study of the role of autophagy in stemness-associated plasticity in breast cancer cells (FeroStem) (PIs: Drs Ahmed HAMAI and Maryam MEHRPOUR)
4. Use animal models of benign prostatic hyperplasia to challenge drug efficacy, elucidate exhaustion of therapeutic effect and identify alternative druggable pathways (PIs: Dr Vincent GOFFIN and Pr Nicolas BARRY DELONGCHAMPS)

5 main publications

• Pigat, N., E. Reyes-Gomez, F. Boutillon, S. Palea, N. Barry Delongchamps, E. Koch and V. Goffin (2019). "Combined Sabal and Urtica Extracts (WS®1541) Exert Anti-proliferative and Anti-inflammatory Effects in a Mouse Model of Benign Prostate Hyperplasia." Front Pharmacol 10: 311.
• Bernichtein, S., N. Pigat, N. Barry Delongchamps, F. Boutillon, V. Verkarre, P. Camparo, E. Reyes-Gomez, A. Mejean, S. M. Oudard, E. M. Lepicard, M. Viltard, J. C. Souberbielle, G. Friedlander, T. Capiod* and V. Goffin* (2017). "Vitamin D3 prevents calcium-induced progression of early-stage prostate tumors by counteracting TRPC6 and calcium sensing receptor upregulation." Cancer Res 77: 355-365.
• *Mai, T. T., *A. Hamai, A. Hienzsch, T. Caneque, S. Muller, J. Wicinski, O. Cabaud, C. Leroy, A. David, V. Acevedo, A. Ryo, C. Ginestier, D. Birnbaum, E. Charafe-Jauffret, P. Codogno, *M. Mehrpour and *R. Rodriguez (2017). "Salinomycin kills cancer stem cells by sequestering iron in lysosomes." Nat Chem 9(10): 1025-1033
• Sackmann Sala, L., F. Boutillon, G. Menara, A. De Goyon-Pelard, M. Leprevost, J. Codzamanian, N. Lister, J. Pencik, A. Clark, N. Cagnard, C. Bole-Feysot, R. Moriggl, G. P. Risbridger, R. A. Taylor, L. Kenner, J. E. Guidotti and V. Goffin (2017). "A rare castration-resistant progenitor cell population is highly enriched in Pten-null prostate tumors." J Pathol 243: 54-64
• Rouet, V., R. L. Bogorad, C. Kayser, K. Kessal, C. Genestie, A. Bardier, D. R. Grattan, B. Kelder, J. J. Kopchick, P. A. Kelly and V. Goffin (2010). "Local prolactin is a target to prevent expansion of basal/stem cells in prostate tumors." Proc Natl. Acad. Sci. U. S. A 107(34): 15199-15204

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