Celio Pouponnot PhD Molecular biologist

Course and current status

A. Professional Experience

2018: DR2 Research Director. Permanent position at CNRS

2015: PI of the team Signaling and tumor progression https://curie.fr/equipe/eychene_pouponnot

2009: Habilitation à Diriger les Recherches. Université Paris XI.

2004: CR1 - Permanent position at CNRS.

2000: CR2 - Permanent position at CNRS. Laboratory of A. Eychène, CNRS UMR 146, Institut Curie.

1997-2000:  Post-Doctoral training on TGFb signaling Laboratory of J. Massagué Memorial Sloan Kettering Cancer Center New York USA..

1996: PhD in Microbiology. University Paris VI. Laboratory of Dr Calothy; CNRS URA 1443 ; Institut Curie.

1992: Master’s degree in Microbiology (speciality : virology). University Paris VI. Course of General Virology, Laboratory of Dr Calothy; CNRS URA 1443 ; Institut Curie.


B. Positions and Honors

2019: Participation Groupe de Travail INCa "Recherche Cancer Pédiatrique"

Since 2019: Member of the Scientific Advisory Board Gefluc IDF

Since 2019: Member of expert committee Cancer Fondation de France

Since 2013: Member of the Scientific Advisory Board of the Interregional ligue Contre le Cancer Grand Ouest (CISRGO)

Since 2017: Member of the steering committee of the IRS NanoTheRad (Supported by IDEX Paris Saclay)

2014-2018: Member of the “Commission Scientifique Nationale n° 4” – Fondation ARC

2016-2019: Member of the board of the Club Hematopoïèse et Oncogénèse – Meeting Organization of the 23rd, 24th, 25th,        26th annual meetings

2016, 2018: Member of the "Review Board" PhD-IC3i (Institut Curie)

2014-2016 and 2018: Member of the Jury Jeunes Chercheurs – Fondation ARC

2012-2016:  Member of the Steering Committee of the Bioinformatic facility of the Institut Curie

Scientific summary

Celio POUPONNOT performed his PhD in G. Calothy's team where he studied the transcriptional regulation of genes in cancer and identified one of the first target genes of MAF transcription factors family (Pouponnot et al., 1995 MCB). He also contributed to the identification and characterization of a new member of this family, the MAFA gene (Benkhelifa et al., 1998 Oncogene). Between 1997 and 2000, he completed a 4-year post-doctoral fellowship in the Memorial Sloan Kettering Cancer Center (MSKCC, New York USA) in the team of Dr J. Massagué, a world leader in the TGFb/Activin / BMP signaling field. He notably described the central role of SMAD4 in these signaling pathways (Liu et al., 1997 Genes & Dev) and studied the mechanisms by which SMAD proteins modulate gene expression (Pouponnot et al., 1998 JBC; Seoane et al., 2001 Nat Cell Biol). He was recruited at the CNRS in 2000 in the A. Eychène's team where he led a research group focusing on the role and regulations of MAF transcription factors. He demonstrated that MAF proteins exhibit a context dependent oncogenic activity, acting both as oncogenes and tumor suppressors (Pouponnot et al., 2006 Oncogene). His team has identified their main phosphorylations which are mediated by the GSK3 kinase and control their activity (Rocques et al., 2007 Mol Cell). These phosphorylations represent a key regulatory process for MAF transcription factors. Mutations which prevent these phosphorylations have been identified in human. They are associated with different syndromes and developmental abnormalities (Niceta et al., 2015 AJHG). His team has also shown that these phosphorylations can be therapeutically targeted in multiple myeloma (Herath et al., 2014 Blood Cancer J). He proposed a model whereby the protumorigenic activity of MAF proteins is uncoupled from their physiological role (Eychène et al., Nat Rev Cancer 2008). Since 2015, he heads the "Signaling and tumor progression" team in the Curie Institute. The proposed model was validated by his team by showing that NRL, an MAF transcription factor plays an essential role in medulloblastoma (MB), a pediatric tumor of the cerebellum. In physiological conditions, NRL is exclusively expressed in photoreceptor cells of the retina and not in the cerebellum. In MB, NRL is involved in MB progression and establishes an abnormal photoreceptor identity by inducing a gene expression program (Garancher et al., 2018 Cancer Cell). This work highlights the role of an abnormal identity unrelated to the tissue of origin in cancer and questions the concept of “lineage addiction” in cancer. The team has also shown the therapeutic value of targeting the TGFb / Activin pathway in MB (Morabito et al., 2019 EMBO Mol Med) The team has developed strong activities and expertise on pediatric tumors of the nervous system, in particular in MB and through collaborations in AT/RT (Leruste et al., 2019 Cancer cell) and retinoblastoma (Liu et al., 2021 Nat Comm). Current projects focus on these cancers by studying signaling pathways and transcription factors involved as well as the efficacy of radiotherapy and its toxicity on normal tissue (Ferreira et al., 2020 CCD).

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