Endophilin-A3 and Galectin-8 control the clathrin-independent endocytosis of CD166

Henri-François Renard (), François Tyckaert, Cristina Lo Giudice, Thibault Hirsch, Cesar Augusto Valades-Cruz, Camille Lemaigre, Massiullah Shafaq-Zadah, Christian Wunder, Ruddy Wattiez, Ludger Johannes, Pierre van der Bruggen, David Alsteens and Pierre Morsomme ()
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Henri-François Renard: UCLouvain, Louvain Institute of Biomolecular Science and Technology, Group of Molecular Physiology
François Tyckaert: UCLouvain, Louvain Institute of Biomolecular Science and Technology, Group of Molecular Physiology
Cristina Lo Giudice: UCLouvain, Louvain Institute of Biomolecular Science and Technology, NanoBiophysics lab
Thibault Hirsch: UCLouvain, de Duve Institute
Cesar Augusto Valades-Cruz: Institut Curie, PSL Research University, Cellular and Chemical Biology unit, U1143 INSERM, UMR3666 CNRS
Camille Lemaigre: UCLouvain, Louvain Institute of Biomolecular Science and Technology, Group of Molecular Physiology
Massiullah Shafaq-Zadah: Institut Curie, PSL Research University, Cellular and Chemical Biology unit, U1143 INSERM, UMR3666 CNRS
Christian Wunder: Institut Curie, PSL Research University, Cellular and Chemical Biology unit, U1143 INSERM, UMR3666 CNRS
Ruddy Wattiez: UMons, Research Institute for Biosciences, Proteomics and Microbiology Lab
Ludger Johannes: Institut Curie, PSL Research University, Cellular and Chemical Biology unit, U1143 INSERM, UMR3666 CNRS
Pierre van der Bruggen: UCLouvain, de Duve Institute
David Alsteens: UCLouvain, Louvain Institute of Biomolecular Science and Technology, NanoBiophysics lab
Pierre Morsomme: UCLouvain, Louvain Institute of Biomolecular Science and Technology, Group of Molecular Physiology

Nature Communications, 2020, vol. 11, issue 1, 1-13

Abstract: Abstract While several clathrin-independent endocytic processes have been described so far, their biological relevance often remains elusive, especially in pathophysiological contexts such as cancer. In this study, we find that the tumor marker CD166/ALCAM (Activated Leukocyte Cell Adhesion Molecule) is a clathrin-independent cargo. We show that endophilin-A3—but neither A1 nor A2 isoforms—functionally associates with CD166-containing early endocytic carriers and physically interacts with the cargo. Our data further demonstrates that the three endophilin-A isoforms control the uptake of distinct subsets of cargoes. In addition, we provide strong evidence that the construction of endocytic sites from which CD166 is taken up in an endophilin-A3-dependent manner is driven by extracellular galectin-8. Taken together, our data reveal the existence of a previously uncharacterized clathrin-independent endocytic modality, that modulates the abundance of CD166 at the cell surface, and regulates adhesive and migratory properties of cancer cells.

Date: 2020
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DOI: 10.1038/s41467-020-15303-y

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