KLK3 in the Regulation of Angiogenesis-Tumorigenic or Not?

Int J Mol Sci. 2021 Dec 17;22(24):13545. doi: 10.3390/ijms222413545.

Abstract

In this focused review, we address the role of the kallikrein-related peptidase 3 (KLK3), also known as prostate-specific antigen (PSA), in the regulation of angiogenesis. Early studies suggest that KLK3 is able to inhibit angiogenic processes, which is most likely dependent on its proteolytic activity. However, more recent evidence suggests that KLK3 may also have an opposite role, mediated by the ability of KLK3 to activate the (lymph)angiogenic vascular endothelial growth factors VEGF-C and VEGF-D, further discussed in the review.

Keywords: KLK3; PSA; VEGF-C; VEGF-D; angiogenesis; cancer; proteolysis.

Publication types

  • Review

MeSH terms

  • Gene Expression Regulation, Neoplastic
  • Humans
  • Kallikreins / metabolism*
  • Male
  • Neovascularization, Pathologic / metabolism*
  • Prostate-Specific Antigen / metabolism*
  • Prostatic Neoplasms / genetics
  • Prostatic Neoplasms / metabolism*
  • Prostatic Neoplasms / physiopathology
  • Vascular Endothelial Growth Factor C
  • Vascular Endothelial Growth Factor D

Substances

  • VEGFC protein, human
  • VEGFD protein, human
  • Vascular Endothelial Growth Factor C
  • Vascular Endothelial Growth Factor D
  • KLK3 protein, human
  • Kallikreins
  • Prostate-Specific Antigen