Angiotensin-(1-7) can promote cell migration and tumor growth of clear cell renal cell carcinoma

P Sobczuk1, J Trzcinska-Danielewicz2, L Koperski3

  • 1Department of Experimental and Clinical Physiology, Laboratory of Centre for Preclinical Research, Medical University of Warsaw, Warsaw, Poland. pawel.sobczuk@wum.edu.pl.

Insights

Angiotensin-(1-7) (Ang-(1-7)) may promote renal cell carcinoma (RCC) growth and migration, contrary to its proposed anticancer effects. Further studies are needed to confirm these protumorigenic findings in diverse RCC models.

Area of Science:

  • Oncology
  • Cardiovascular Research
  • Renal System Physiology

Background:

  • Renal cell carcinoma (RCC) is a prevalent kidney cancer with increasing drug resistance.
  • Angiotensin-(1-7) (Ang-(1-7)), a renin-angiotensin system peptide, shows conflicting efficacy as an anticancer agent.
  • Investigating Ang-(1-7)'s role in RCC is crucial due to its potential therapeutic implications.

Purpose of the Study:

  • To evaluate the effects of Ang-(1-7) on renal cell carcinoma (RCC) cell lines in vitro.
  • To assess the in vivo impact of Ang-(1-7) on RCC tumor growth using a mouse xenograft model.
  • To clarify the conflicting data regarding Ang-(1-7)'s efficacy against RCC.

Main Methods:

  • In vitro studies on Caki-1 and Caki-2 cell lines to assess cell viability and migration.
  • In vivo xenograft study using Caki-1 cells in nude mice to evaluate tumor growth.
  • Investigation of Mas receptor (MasR) activation and its role in Ang-(1-7) effects.

Main Results:

  • Ang-(1-7) did not affect cell viability but promoted cell migration in RCC cell lines.
  • In vivo, Ang-(1-7) enhanced tumor growth, an effect not blocked by MasR antagonism.
  • No significant impact on cell proliferation or tumor vessel density was observed.

Conclusions:

  • Angiotensin-(1-7) demonstrates potential protumorigenic activity in renal cell carcinoma models.
  • The pro-tumorigenic effects of Ang-(1-7) may involve Mas receptor-independent pathways.
  • Further research across diverse RCC models is necessary to understand its complex role and the disease's heterogeneity.

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