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Updated: May 9, 2026

Modeling Spontaneous Metastatic Renal Cell Carcinoma (mRCC) in Mice Following Nephrectomy
Published on: April 29, 2014
The renin-angiotensin system as a target of novel anticancer therapy
Katarzyna Regulska1, Beata Stanisz, Milosz Regulski
1Greater Poland Oncology Center, 15th Garbary Street, 61-866 Poznan, Poland. katarzyna.regulska@wco.pl.
Abstract:
The role of the renin-angiotensin system (RAS) in the development of various malignancies has recently been extensively examined and, since it has been shown to significantly influence many aspect of cancer initiation and progression, the idea of RAS-targeted anticancer therapy has arisen. This article reviews the mechanisms underlying RAS-induced physiological and pathological responses related to cancer biology, including tumor growth, cell proliferation, apoptosis, angiogenesis, inflammation, and protein degradation, emphasizing the associated cellular transduction schemes activated by main RAS effectors. Also the dual nature of RAS-dependent effects, resulting from its complex physiology has been commented. Finally, based on the available data from clinical trials and experimental studies, the possibilities of the introduction of RAS-modulating drugs into standard clinical practice in oncology have been discussed with the focus on both, positive and negative effects associated with the administration of various classes of pharmaceuticals to cancer patients.
Insights
The renin-angiotensin system (RAS) impacts cancer growth and progression. Targeting RAS with drugs shows potential for anticancer therapy, but clinical use requires careful consideration of benefits and risks.
Area of Science:
- Oncology
- Pharmacology
- Physiology
Background:
- The renin-angiotensin system (RAS) plays a significant role in cancer initiation and progression.
- RAS influences key cancer processes like tumor growth, proliferation, and angiogenesis.
Purpose of the Study:
- To review RAS mechanisms in cancer biology.
- To discuss the potential of RAS-targeted anticancer therapies.
- To evaluate clinical data on RAS-modulating drugs in oncology.
Main Methods:
- Literature review of experimental studies and clinical trials.
- Analysis of cellular transduction pathways activated by RAS effectors.
- Discussion of the dual nature of RAS-dependent effects in cancer.
Main Results:
- RAS significantly affects tumor growth, cell proliferation, apoptosis, angiogenesis, inflammation, and protein degradation.
- RAS-modulating drugs show potential but also present risks.
- The complex physiology of RAS results in dual effects on cancer.
Conclusions:
- RAS is a key player in cancer development and progression.
- RAS-targeted therapies offer a promising avenue for cancer treatment.
- Careful evaluation of both positive and negative effects of RAS-modulating drugs is crucial for clinical application.
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