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Updated: Aug 2, 2025

Comparing Metastatic Clear Cell Renal Cell Carcinoma Model Established in Mouse Kidney and on Chicken Chorioallantoic Membrane
Published on: February 8, 2020
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.
Abstract:
Renal cell carcinoma (RCC) is the most common kidney malignancy, accounting for 3% of all cancers. Despite significant advances in targeted therapies and immunotherapy, many patients with RCC develop resistance to available drugs. Angiotensin-(1-7) (Ang-(1-7)) is a heptapeptide and a member of the renin-angiotensin system which regulates the cardiovascular and the renal system. It has been proposed as a potential anticancer agent for the treatment of various types of cancers, but data regarding its efficiency against RCC are conflicting. The aim of our study was to evaluate the effects of Ang-(1-7) in RCC models in vitro and in vivo. We performed a series of in vitro experiments investigating the effects of Ang-(1-7) on cell viability and migration in Caki-1 and Caki-2 cell lines. In addition, we carried out an in vivo study in xenografts of Caki-1 cells in nude mice. In results: Ang-(1-7) or A779, an antagonist of its receptor MasR (Mas receptor), showed no effect on cell viability. Ang-(1-7) promoted cell migration in a dose-dependent manner by inducing the activation of MasR. It also promoted tumor growth in vivo, and this effect was not inhibited by the blockade of MasR. No effects on cell proliferation or tumor vessel density were observed. The results suggest that Ang-(1-7) can exert protumorigenic activity in RCC, however, further research on other RCC models is needed to better recapitulate the heterogeneity of the disease.
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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