Multitasking discoidin domain receptors are involved in several and specific hallmarks of cancer

Cell Adh Migr. 2018;12(4):363-377. doi: 10.1080/19336918.2018.1465156. Epub 2018 Jun 8.

Abstract

Discoidin domain receptors, DDR1 and DDR2, are two members of collagen receptor family that belong to tyrosine kinase receptor subgroup. Unlike other matrix receptor-like integrins, these collagen receptors have not been extensively studied. However, more and more studies are focusing on their involvement in cancer. These two receptors are present in several subcellular localizations such as intercellular junction or along type I collagen fibers. Consequently, they are involved in multiple cellular functions, for instance, cell cohesion, proliferation, adhesion, migration and invasion. Furthermore, various signaling pathways are associated with these multiple functions. In this review, we highlight and characterize hallmarks of cancer in which DDRs play crucial roles. We discuss recent data from studies that demonstrate the involvement of DDRs in tumor proliferation, cancer mutations, drug resistance, inflammation, neo-angiogenesis and metastasis. DDRs could be potential targets in cancer and we conclude this review by discussing the different ways to inhibits them.

Keywords: STED microscopy; fenestrae; livers sinusoidal endothelial cells (LSEC).

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Discoidin Domain Receptors / metabolism*
  • Drug Resistance, Neoplasm
  • Humans
  • Models, Biological
  • Neoplasms / blood supply
  • Neoplasms / metabolism*
  • Signal Transduction

Substances

  • Discoidin Domain Receptors

Grants and funding

E. Henriet and M. Sala are supported by a PhD from the Ministère de l'Enseignement Supérieur et de la Recherche. This work has been supported by grants from SIRIC BRIO, ARC, La Ligue Nationale contre le Cancer. F. Saltel and V. Moreau are supported by fundings from Equipe Labellisée, Ligue Nationale contre le Cancer 2016, SIRIC BRIO and INCA, PLBIO15-135 (to FS) and PLBIO2014-182 (to VM).