Fabrice Fleury

Prof. Fabrice Fleury

CNRS UMR 6286, Nantes Université, Nantes, Pays de la Loire, France

Research Focus & Metrics

Academic Career Length

21Years (2006-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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Sarah MéresseSarah Méresse
Sarah Méresse
Mostefa FODILMostefa FODIL
Mostefa FODIL
FFFabrice Fleury
Fabrice Fleury
Benoît ChénaisBenoît Chénais
Benoît Chénais
Fucoxanthin is a well-known carotenoid of the xanthophyll family, mainly produced by marine organisms such as the macroalgae of the fucus genus or microalgae such as Phaeodactylum tricornutum. Fucoxanthin has antioxidant and anti-inflammatory properties but also several anticancer effects. Fucoxanthin induces cell growth arrest, apoptosis, and/or autophagy in several cancer cell lines as well as in animal models of cancer. Fucoxanthin treatment leads to the inhibition of metastasis-related migration, invasion, epithelial–mesenchymal transition, and angiogenesis. Fucoxanthin also affects the DNA repair pathways, which could be involved in the resistance phenotype of tumor cells. Moreover, combined treatments of fucoxanthin, or its metabolite fucoxanthinol, with usual anticancer treatments can support conventional therapeutic strategies by reducing drug resistance. This review focuses on the current knowledge of fucoxanthin with its potential anticancer properties, showing that fucoxanthin could be a promising compound for cancer therapy by acting on most of the classical hallmarks of tumor cells.

20 November 2015 in Biomolecules
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DVDenis Velic
Denis Velic
ACAnthony Couturier
Anthony Couturier
MFMaria Ferreira
Maria Ferreira
ARAmélie Rodrigue
Amélie Rodrigue
GPGuy G. Poirier
Guy G. Poirier
JMJean-Yves Masson
Jean-Yves Masson
For decades, radiotherapy and chemotherapy were the two only approaches exploiting DNA repair processes to fight against cancer. Nowadays, cancer therapeutics can be a major challenge when it comes to seeking personalized targeted medicine that is both effective and selective to the malignancy. Over the last decade, the discovery of new targeted therapies against DNA damage signalling and repair has offered the possibility of therapeutic improvements in oncology. In this review, we summarize the current knowledge of DNA damage signalling and repair inhibitors, their molecular and cellular effects, and future therapeutic use.

1 December 2021 in Biochimica et Biophysica Acta (BBA) - Reviews on Cancer
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ADA. Demeyer
A. Demeyer
HBH. Benhelli-Mokrani
H. Benhelli-Mokrani
Benoît ChénaisBenoît Chénais
Benoît Chénais
PWP. Weigel
P. Weigel
FFFabrice Fleury
Fabrice Fleury

9 November 2016 in Medicinal Chemistry Research
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IYIvan Yaremenko
Ivan Yaremenko
MSMikhail Syroeshkin
Mikhail Syroeshkin
DLDmitri O. Levitsky
Dmitri O. Levitsky
FFFabrice Fleury
Fabrice Fleury
Alexander Terent'evAlexander Terent'ev
Alexander Terent'ev

23 March 2019 in Cancers
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TCThomas Chabot
Thomas Chabot
ADAlain Defontaine
Alain Defontaine
DMDamien Marquis
Damien Marquis
ARAxelle Renodon-Corniere
Axelle Renodon-Corniere
ECEmmanuelle Courtois
Emmanuelle Courtois
YCYvonnick Cheraud
Yvonnick Cheraud
Genomic instability through deregulation of DNA repair pathways can initiate cancer and subsequently result in resistance to chemo and radiotherapy. Understanding these biological mechanisms is therefore essential to overcome cancer. RAD51 is the central protein of the Homologous Recombination (HR) DNA repair pathway, which leads to faithful DNA repair of DSBs. The recombinase activity of RAD51 requires nucleofilament formation and is regulated by post-translational modifications such as phosphorylation. In the last decade, studies have suggested the existence of a relationship between receptor tyrosine kinases (RTK) and Homologous Recombination DNA repair. Among these RTK the c-MET receptor is often overexpressed or constitutively activated in many cancer types and its inhibition induces the decrease of HR. In this study, we show for the first time that c-MET is able to phosphorylate the RAD51 protein. We demonstrate in vitro that c-MET phosphorylates four tyrosine residues localized mainly in the subunit-subunit interface of RAD51. Whereas these post-translational modifications do not affect the presynaptic filament formation, they strengthen its stability against the inhibitor effect of the BRC peptide obtained from BRCA2. Taken together, these results confirm the role of these modifications in the regulation of the BRCA2-RAD51 interaction and underline the importance of c-MET in DNA damage response.

3 August 2018 in New Journal of Chemistry
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KDKonstantin V. Deriabin
Konstantin V. Deriabin
IYIvan Yaremenko
Ivan Yaremenko
MCMikhail Chislov
Mikhail Chislov
FFFabrice Fleury
Fabrice Fleury
Alexander Terent'evAlexander Terent'ev
Alexander Terent'ev
RIRegina M. Islamova
Regina M. Islamova
Cyclic organosilicon triperoxides were found to be vinyl-selective free-radical initiators for thermal curing at 100–180 °C of vinyl-terminated polydimethylsiloxane and trimethylsilyl-terminated polymethylhydrosiloxane producing homogeneous transparent silicone rubbers with antibacterial properties. The usage of the cyclic organosilicon triperoxides as the curing agents does not require free radical inhibitors in comparison with diacyl- and dialkyl peroxides. Among the tested compounds, the peroxide with the Me–Si–Me fragment and two cyclohexane rings is a much more active curing agent (180 °C, c = 0.22 M, τcuring = 45 min) than other organosilicon peroxides. Cured silicone samples from mixtures with vinyl-terminated polysiloxane and silicone hydride have improved mechanical properties: peroxides provide more than 200% elongation, and compression sets of the samples are less than 1%. The prepared silicone rubbers showed pronounced antibacterial activity.