Magali Trayssac

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MAGALI TRAYSSAC – POSTDOCTORAL ASSOCIATE

The Lipid Cancer Lab

MART (Medical and Research Translation) Building

9th floor, south

100 Nicolls Road

Stony Brook, NY 11794-7294

magali.trayssac@stonybrookmedicine.edu

631-216-8318

 

Education:

PhD in Pathophysiology, 2014, Toulouse, France

MS in Biology and Health, 2009, Toulouse, France

BS in Life and Health Sciences, 2007, Toulouse, France

 

Main project:

I focus my research on cellular senescence, mechanism by which cells stop dividing and enter a prolonged cell cycle arrest. In the context of cancer, it can be triggered by many inducers such as oncogenes and chemotherapeutic drugs. Senescence participates in the prevention of tumor development and progression, especially in early stages. Its role is more controversial in late stages of the disease.

My main project is to study the role of sphingosine kinase 1 (SK1) in oncogene-induced senescence. SK1 is a master regulator of the sphingolipid metabolism and cancer cell biology because it phosphorylates sphingosine (Sph) to form sphingosine-1-phosphate (S1P). Sph, as well as ceramide (Cer) another major sphingolipid, have anti-cancer properties leading to cell death and senescence, whereas S1P shows pro-cancer effects triggering cell proliferation and migration and delaying senescence induction.

SK1 is upregulated in many cancers and we hypothesize that oncogenes lead to an increase of SK1 activity/expression in order to escape from tumor senescence. We believe that targeting SK1 is an efficient way to enhance oncogene-induced senescence and to prevent cancer cell proliferation. We are working on identifying the sphingolipids and sphingolipid enzymes involved in this biology.

Publications:

Bioactive Sphingolipids: Advancements and Contributions from the Laboratory of Dr. Lina M. Obeid.
Velazquez FN, Hernandez-Corbacho M, Trayssac M, Stith JL, Bonica J, Jean B, Pulkoski-Gross MJ, Carroll BL, Salama MF, Hannun YA, Snider AJ.
Accepted in Cellular Signaling, Dec 2020. Review

Increased cell growth during serine starvation through mitochondrial accumulation of sphingosine.
Truman JP, Ruiz CF, Trayssac M, Mao C, Hannun YA, Obeid LM.
Accepted in The FASEB Journal, Dec 2020.

Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides.
Trayssac M, Clarke CJ, Stith JL, Snider JM, Newen N, Gault CR, Hannun YA, Obeid LM.
Accepted in Cell Death & Disease, Nov 2020.

Multiple actions of doxorubicin on the sphingolipid network revealed by flux analysis.
Snider JM, Trayssac M, Clarke CJ, Schwartz N, Snider AJ, Obeid LM, Luberto C, Hannun YA.
Journal of Lipid Research. 2019 Apr;60(4):819-831.

Role of sphingolipids in senescence: implication in aging and age-related diseases.
Trayssac M, Hannun YA, Obeid LM.
Journal of Clinical Investigation. 2018 July 2;128(7):2702-2712. Review

Role of sphingosine-1-phosphate in transplant vasculopathy evoked by anti-HLA antibody. 
Trayssac M, Galvani S, Augé N, Sabbadini R, Calise D, Mucher E, Sallusto F, Thomsen M, Salvayre R, Nègre-Salvayre A.
American Journal of Transplantation. 2015 Aug;15(8):2050-61.

Oxidized LDL-induced angiogenesis involves sphingosine-1-phosphate: prevention by anti-S1P antibody.
Camaré C, Trayssac M, Garmy-Susini B, Mucher E, Sabbadini R, Salvayre R, Nègre-Salvayre R.
British Journal of Pharmacology. 2015 Jan;172(1):106-18.

Mechanisms of human smooth muscle cell proliferation and transplant vasculopathy induced by HLA class I antibodies: In vitro and in vivo studies.
Trayssac M, Nègre-Salvayre A, Thomsen M.
Human Immunology. 2012 Dec;73(12):1253-60. Review

A key role for matrix metalloproteinases and neutral sphingomyelinase-2 in transplant vasculopathy triggered by anti-HLA antibody.
Galvani S*, Trayssac M*, Augé N, Thiers JC, Calise D, Krell HW, Sallusto F, Kamar N, Rostaing L, Thomsen M, Nègre-Salvayre A, Salvayre R.
Circulation. 2011 Dec 13;124(24):2725-34.