CV Science

Frederic Delom AGR, ProTeostasis & Cellular plaSticity (ARTiSt)

Course and current status

From 2022 - : Team leader - “Reprograming tumour activity & associated microenvironment”. Inserm U1312.

From 2019 - : Scientific Director -  “PhenOtypic scrEening TechnICal” (POETIC)

From 2016 - : Head of the research group “AGR, ProTeostasis & Cellular plaSticity” (ARTiSt) laboratory.

From 2016 - : Assistant Professor, University of Bordeaux, Bordeaux.

2011- 2016: University-Inserm chair, University of Bordeaux, Bordeaux

2007 - 2010: Post-doctoral position, Barts and The London, London, UK.

2004 - 2006: Post-doctoral position, McGill University, Montreal, Canada.

2001 - 2004: Scientist position, Aventis Pharmaceutical Company, Paris, France.

1998 - 2001: PhD Thesis, INSERM U38, Marseille, France.

Scientific summary

The ARTiSt (AGR, ProTeostasis & Cellular plaSticity) Lab primarily focuses on investigating the responses to endoplasmic reticulum (ER) stress in cancer development. Specifically, the lab aims to understand how ER stress responses, particularly those related to proteostasis and cell plasticity, can be exploited to identify new biomarkers, new therapeutic targets, and ultimately new therapeutic strategies.

Research Project: Cancer progression involves the adaptation of tumour cells to a multitude of both intrinsic and extrinsic factors. Some of these adaptations are, in part, driven by ER stress responses to control proteostasis and cellular plasticity. We have demonstrated an interaction of ER stress with proteostasis and cell plasticity through the Anterior Gradient (AGR) family. AGR proteins belong to the ER-resident PDI family, essential for ER homeostasis. Moreover, they can relocate to the cytosol or extracellular microenvironment, gaining pro-oncogenic functions.

The aims of our research project are as follows:

1.       Investigate mechanisms by which proteostasis reprogramming, induced by ER stress, is signalled throughout the cell and its immune microenvironment.

2.       Investigate the role of ER stress in the reprogramming of tumour cell plasticity, particularly concerning epithelial-mesenchymal transition (EMT) and senescence phenotypes, within the framework of therapy resistance.