Renin-angiotensin inhibitors reprogram tumor immune microenvironment: A comprehensive view of the influences on anti-tumor immunity

The cover for issue 84 of Oncotarget features Figure 2, "Renin-angiotensin inhibitors reprogram tumor immune microenvironment," by Zhu, et al.

The mechanisms by which RASi impair tumor growth extend beyond their function of modulating tumor vasculature.

Dr. Dora L. Vallejo-Ardila from the Department of Surgery, Austin Health, at the University of Melbourne, in Melbourne,VIC 3084, Australia said, "The main components of the conventional axis of the renin-angiotensin system, function as an intricate peptide signaling network through several receptors."

"The main components of the conventional axis of the renin-angiotensin system, function as an intricate peptide signaling network through several receptors."

- Dr. Dora L. Vallejo-Ardila, Department of Surgery, Austin Health, at the University of Melbourne

Figure 2: Renin-angiotensin inhibitors reprogram tumor immune microenvironment. The pathological processes and cellular functions inside the tumor microenvironment which appear to be influenced by RASi include tumor angiogenesis, hypoxia and acidosis within the tumor stroma, inflammatory signaling pathways, oxidative stress, immune cell modulation and the role of kalli krein kinin system (KKS).

ACE2 is mostly found in the vascular endothelial cells and renal tubular epithelium ACE2 cleaves Ang II to Ang-, whereas ACE produces Ang- by cleaving Ang-. Ang II interacts with two different receptors, angiotensin II type 1 receptor and angiotensin II type 2 receptor. ACE2 cleaves Ang II to Angiotensin, whereas ACE produces Ang by cleaving Angiotensin. Angiotensin II is metabolized to Angiotensin III by aminopeptidase A , whereas Ang III is metabolized to Angiotensin IV by aminopeptidase N.

In general, the over-expression of RAS components within the Ang II/AT1R axis is associated with tumor growth and with more aggressive tumor features in several types of human cancer, including breast cancer, ovarian cancer and renal cancer, whereas Ang II/AT2R and Ang /Mas R showed opposite effects.

The Dora L. Vallejo-Ardila research team concluded, "Disease-associated genetic mutation can have an effect on baseline cellular autophagy rates as demonstrated in V600E mutation of BRAF and this could make autophagy modulation particularly useful in affected cells."

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DOI - https://doi.org/10.18632/oncotarget.26174

Full text - https://www.oncotarget.com/article/26174/text/

Correspondence to - Dora L. Vallejo-Ardila - dvallejo@student.unimelb.edu.au

Keywords - renin-angiotensin system, tumor microenvironment, anti-tumor immunity, kallikrein kinin system

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