Abstract
The mechanistic involvement of the renin-angiotensin system (RAS) reaches beyond cardiovascular physiopathology. Recent knowledge pinpoints a pleiotropic role for this system, particularly in the lung, and mainly through locally regulated alternative molecules and secondary pathways. Angiotensin peptides play a role in cell proliferation, immunoinflammatory response, hypoxia and angiogenesis, which are critical biological processes in lung cancer. This manuscript reviews the literature supporting a role for the renin-angiotensin system in the lung tumor microenvironment and discusses whether blockade of this pathway in clinical settings may serve as an adjuvant therapy in lung cancer.
Highlights
Lung cancer is one of the most common malignancies and the most frequent cause of cancer deaths in the past few decades, with over one million people diagnosed worldwide each year [1,2].Notably, the five-year survival rate is the lowest compared with other frequent malignancies [3]
Lewis lung carcinoma cells with Angiotensin II (Ang II) caused a significant increase in vascular endothelial growth factor (VEGF)-A mRNA and protein, which was prevented with administration of an AT1 receptor antagonist [99]
The renin-angiotensin system (RAS) regulates all these capabilities, most prominent are its effects on angiogenesis, invasion, pro-survival signaling and proliferation
Summary
Lung cancer is one of the most common malignancies and the most frequent cause of cancer deaths in the past few decades, with over one million people diagnosed worldwide each year [1,2]. The renin-angiotensin-aldosterone system is an established primary regulator of blood pressure, homeostasis, and natriuresis [4]. Recent evidence indicates that angiotensin peptides might have a role in tumor cell proliferation, inflammation and hypoxia, which have been recognized as hallmarks of cancer, actively participating in lung tumor microenvironment regulation [5]. We review current knowledge on the renin-angiotensin system (RAS), considering its potential modulatory role on cancer cell phenotype and on immune surveillance, while exploring the mechanistic association with lung cancer.
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