The opposite effects of angiotensin 1-9 and angiotensin 3-7 in prostate epithelial cells

Kamila Domińska1, Karolina Kowalska2, Dominika Ewa Habrowska-Górczyńska2

  • 1Department of Comparative Endocrinology, Medical University of Lodz, Lodz, 90-752, Poland.

Insights

Angiotensin-1-9 (Ang1-9) promotes prostate cancer cell growth and migration, while Angiotensin-3-7 (Ang3-7) inhibits these processes. Further research is needed to identify the specific angiotensin receptors involved.

Area of Science:

  • Oncology
  • Molecular Biology
  • Endocrinology

Background:

  • Renin-angiotensin system (RAS) components are implicated in cancer development, including prostate cancer.
  • Specific angiotensin peptides' roles in prostate cancer are not fully understood.

Purpose of the Study:

  • To investigate the effects of Angiotensin-1-9 (Ang1-9) and Angiotensin-3-7 (Ang3-7) on prostate epithelial cell viability, proliferation, migration, and invasion.
  • To explore the impact of these peptides on gene expression related to cancer progression and angiotensin receptors.

Main Methods:

  • In vitro studies on prostate epithelial cells (PNT1A).
  • Assays for cell viability, proliferation, migration, and invasion.
  • Quantitative analysis of gene expression for vascular endothelial growth factor (VEGF), hypoxia-inducible factors (HIF-1), vimentin (VIM), REL proto-oncogene (REL), and angiotensin receptors.

Main Results:

  • Ang1-9 demonstrated pro-cancer effects, increasing cell division, motility, and expression of VEGF, HIF-1, VIM, and REL.
  • Ang3-7 exhibited no mitogenic activity and inhibited PNT1A cell migration, likely by downregulating VEGF and VIM.
  • Both peptides modulated gene expression for angiotensin receptors, but the specific receptor involved in PNT1A cell signaling remains unidentified.

Conclusions:

  • Ang1-9 and Ang3-7 have opposing effects on prostate cancer cell behavior in vitro.
  • Ang1-9 may promote prostate cancer progression, whereas Ang3-7 might have inhibitory effects.
  • Further investigation is required to elucidate the specific angiotensin receptor pathways mediating these effects in prostate cancer.

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