CD105 (Endoglin): A Potential Anticancer Therapeutic Inhibits Mitogenesis and Map Kinase Pathway Activation

Anticancer Res. 2021 Mar;41(3):1219-1229. doi: 10.21873/anticanres.14879.

Abstract

Background: CD105 is highly expressed on human activated endothelial cells (ECs), is an important component of the TGF-β1 receptor complex and is essential for angiogenesis. CD105 expression is up-regulated in activated ECs and is an important potential marker for cancer prognosis.

Materials and methods: In vitro rat myoblasts transfected with the L-CD105 and S-CD105 transfectants. The transfectants were treated with TGF-β1 for the angiogenesis study.

Results: L-CD105 affects cell proliferation in the presence and absence of TGF-β1, and inhibits p-ERK1/2, p-MEK1/2 and p-c-Jun in L-CD105 transfectants compared to controls. The induction of phospho-ERK1/2 following treatment with TGF-β1 remained significantly lower in L-CD105 transfectants compared to controls.

Conclusion: L-CD105 inhibits the phosphorylation of ERK1/2, MEK1/2, c-Jun1/2/3, and associated signalling intermediates. CD105 modulates cell growth and TGF-β1 induced cell signalling through ERK-c-Jun expression.

Keywords: CD105; MAPK; TGF-β1; angiogenesis; cell signalling.

MeSH terms

  • Animals
  • Cell Proliferation
  • Cells, Cultured
  • Endoglin / physiology*
  • Extracellular Signal-Regulated MAP Kinases / physiology
  • Humans
  • MAP Kinase Signaling System / physiology*
  • Neoplasms / blood supply
  • Neoplasms / prevention & control*
  • Neovascularization, Pathologic / etiology
  • Phosphorylation
  • Rats
  • Transforming Growth Factor beta1 / pharmacology

Substances

  • ENG protein, human
  • Endoglin
  • Transforming Growth Factor beta1
  • Extracellular Signal-Regulated MAP Kinases