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Journal of Biomedical Research | Volume: 29
November 19-20, 2018 | Paris, France
Molecular Biology, Tissue Science and Regenerative Medicine
International Conference on
Joint Event
&
4
th
World Heart Congress
The extracellular matrix molecule tenascin-C promotes metastasis by multiple mechanisms
Gertraud Orend
Université de Strasbourg, France
T
oday, an orchestrating role of the tumormicroenvironment
iswidely acceptedwhereespecially stromal cells and soluble
factors are recognized as active players. Yet, the extracellular
matrix, although highly abundant, is often considered as
passive bystander. A better understanding of the functions of
the extracellular matrix in cancer is largely hampered by the
lack of relevant models. This applies also to the extracellular
matrix molecule tenascin-C, which is a marker of the cancer
specific tumor microenvironment. We used a comprehensive
approach comprising novel immune competentmousemodels
(with engineered tenascin-C levels) and demonstrated that
tenascin-Cplaysmultiple roles incancer. Tenascin-C is dangerous
as soon as it is expressed out of control. Through assembly into
“Tumor Matrix Tracks”, tenascin-C impacts tumor and stromal
cells including immune cells thereby regulating tumor immunity.
Tenascin-C also enhances formation of new but leaky blood
vessels. Direct interactions with tenascin-C causes endothelial
cell rounding and death or survival upon induction of an
insulatingpericellular fibronectin coat. Tenascin-Cenhances the
angiogenic switch and upregulates a proangiogenic secretome.
Finally, tenascin-C is an important component of metastatic
vascular invasions by promoting endothelialization and cellular
plasticity thereby increasing lung metastasis.
e:
gertraud.orend@inserm.frMolecular Biology & Heart Congress 2018, Volume 29
DOI: 10.4066/biomedicalresearch-C8-023