158P - Renin Angiotensin System (RAS) blockade attenuates growth and metastasis formation of renal cell carcinoma in mice

Date 28 September 2014
Event ESMO 2014
Session Poster Display session
Topics Renal Cell Cancer
Cancer Biology
Basic Scientific Principles
Presenter Wedson Araujo
Citation Annals of Oncology (2014) 25 (suppl_4): iv53-iv57. 10.1093/annonc/mdu325
Authors W. Araujo1, M. Naves2, J.N. Ravanini3, V. Teixeira2
  • 1Pathology, Federal University of São Paulo, 04023-900 - SAO PAULO/BR
  • 2Nephrology, São Paulo Federal University, 04023-900 - São Paulo/BR
  • 3Pathology, São Paulo University, 01246-903 - SAO PAULO/BR



Renal cell carcinoma (RCC) is the most frequent cancer among renal neoplasms in adults and poorly responsive to radio-, chemo- and immunotherapy. There is increasing evidence that blockade of RAS has antineoplasic effects. Objective: Investigate the effects of RAS blockade on renal cell carcinoma (RCC) in a murine model.


Murine renal cancer cells (RENCA) were cultivated and injected (1x105) into subcapsular space of the left kidney of BALB/c mice (8 weeks). The animals were divided into 4 groups : control group (no treatment), Losartan (100 mg / kg / day), Captopril group (10 mg / kg / day) and Losartan + Captopril group (100 mg / kg / day + 10 mg / kg / day). The animals received the drugs by gavage 2 days before tumor induction and continued until euthanasia (21 days after inoculation). After sacrifice, kidneys and lungs were removed, weighed and processed for histopathological analysis. Angiogenesis and vascular microvessel were determined by immunohistochemical evaluation for VEGF and CD34.


All inoculated animals developed renal tumors. Treated animals presented smaller tumors, regardless of the therapeutic regimen, and far fewer lung metastases in both quantity and dimension in relation to controls. The expressions of VEGF and CD34 were significantly decreased in renal tumors of animals treated compared with controls.


Our findings suggest that blockade of RAS decreases the tumor proliferation capacity and metastatic potential of renal cell carcinoma in this experimental model.


All authors have declared no conflicts of interest.