TGF-β superfamily co-receptors in cancer.

Journal Article (Journal Article;Review)

Transforming growth factor-β (TGF-β) superfamily signaling via their cognate receptors is frequently modified by TGF-β superfamily co-receptors. Signaling through SMAD-mediated pathways may be enhanced or depressed depending on the specific co-receptor and cell context. This dynamic effect on signaling is further modified by the release of many of the co-receptors from the membrane to generate soluble forms that are often antagonistic to the membrane-bound receptors. The co-receptors discussed here include TβRIII (betaglycan), endoglin, BAMBI, CD109, SCUBE proteins, neuropilins, Cripto-1, MuSK, and RGMs. Dysregulation of these co-receptors can lead to altered TGF-β superfamily signaling that contributes to the pathophysiology of many cancers through regulation of growth, metastatic potential, and the tumor microenvironment. Here we describe the role of several TGF-β superfamily co-receptors on TGF-β superfamily signaling and the impact on cellular and physiological functions with a particular focus on cancer, including a discussion on recent pharmacological advances and potential clinical applications targeting these co-receptors.

Full Text

Duke Authors

Cited Authors

  • Pawlak, JB; Blobe, GC

Published Date

  • January 2022

Published In

Volume / Issue

  • 251 / 1

Start / End Page

  • 137 - 163

PubMed ID

  • 33797167

Pubmed Central ID

  • PMC8484463

Electronic International Standard Serial Number (EISSN)

  • 1097-0177

Digital Object Identifier (DOI)

  • 10.1002/dvdy.338


  • eng

Conference Location

  • United States