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The aim of this work is to evaluate the sensitizer potential to antitumoral treatments of a new compound: S-nitrosocaptopril. This molecule possesses a NO moeity and an ACE inhibitor ability. Based on previous studies, we have hypothesized that S-nitrosocaptopril can increase the sensibilisation of tumor by increasing the 02 availability and decreasing the cellular respiration rate. We have investigated this effect by RPE spectryoscopy and MRI. We first evaluated the effect of tumor oxygenation by RPE L-band and have confirmed these results by 19F-MRI. The S-nitrosocaptopril has led to an increase of p02 after thirty minutes and the pression pressure was maintained during thirty more minutes. We have then searched the mechanism by investigating the tumor perfusion by patent blue staining. There was no difference between captopril and S­ nitrosocaptopril , perhaps because the captopril has elevated too much the blood flow to see any variation. After that, we have tested the ability of S-nitrosocaptopril to inhibit the oxygen consumption in vitro by EPR X-band spectrometer. There was a significant difference between the both treatments and the S-nitrosocaptopril consumes less oxygen than the captopril. We wanted to highlight the presence of NO by spin-trapping but this experiment failed. However, we have found that theS-nitrosocaptopril is superior to the captopril in their effect to increase the p02 in the tumor. It comes from decreasing the consumption of oxygen. The radio- and chemo sensitizer effect of S-nitrosocaptopril need still to be evaluated by assaying tumor regrowth delay assay.

Captopril --- S-nitrosocaptopril --- Tumor Microenvironment

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

microenvironment --- extracellular matrix --- disease --- cancer --- aging

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This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact

Medicine --- Immunology --- tumor microenvironment --- monocyte --- macrophage --- neutrophil --- immunosuppression --- immunotherapy --- tumor microenvironment --- monocyte --- macrophage --- neutrophil --- immunosuppression --- immunotherapy

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cancer biology --- metastasis --- cancer microenvironment --- tumor metabolism --- molecular mechanisms

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The biological outcome of Hyaluronan (also hyaluronic acid, abbreviated HA) interaction with its CD44 or RHAMM receptors recently attracted much attention within the scientific community owing to a Nature article by Tian X et al. (Nature 2013; 499:346-9). The article described a life span exceeding 30 years in naked mole rats, whereas the maximal lifespan of mice, to which the naked mole rat is related, is only 4 years. This observation is accompanied by the finding that the naked mole rat, in contrast to the mouse, does not develop spontaneous tumors during this exceptional longevity. The article provides evidence that interaction of long tissue HA (6000-12,000 kDa) of the naked mole rat with cell surface CD44, in contrast to the interaction of short tissue HA (less than 3000 kDa) with the mouse CD44, makes the difference. More specifically, this communication shows that the interaction of short HA with fibroblasts’ CD44 imposes on them susceptibility for malignant transformation, whereas the corresponding interaction with long HA imposes on the fibroblasts a resistance to malignant transformation. The article does not explain the mechanism that underlines these findings. However, the articles, that will be published in the proposed Research Topic in the Inflammation section of Frontiers in Immunology, can bridge not only this gap, but also may explain why interaction between short HA and cell surface CD44 (or RHAMM, an additional HA receptor) enhances the development of inflammatory and malignant diseases. Furthermore, the articles included in the proposed Frontiers Research Topic will show that cancer cells and inflammatory cells share several properties related to the interaction between short HA and cell surface CD44 and/or RHAMM. These shared properties include: 1. Support of cell migration, which allows tumor metastasis and accumulation of inflammatory cells at the inflammation site; 2. Delivery of intracellular signaling, which leads to cell survival of either cancer cells or inflammatory cells; 3. Delivery of intracellular signaling, which activates cell replication and population expansion of either cancer cells or inflammatory cells; and 4. Binding of growth factors to cell surface CD44 of cancer cells or inflammatory cells (i.e., the growth factors) and their presentation to cells with cognate receptors (endothelial cells, fibroblasts), leading to pro-malignant or pro-inflammatory activities. Going back to the naked mole rat story, we may conclude from the proposed articles of this Frontiers Research Topic that the long HA, which displays anti-malignant effect, interferes with the above described pro-malignant potential of the short HA (perhaps by competing on the same CD44 receptor). Extrapolating this concept to Inflammation, the same mechanism (competition?) may be valid for inflammatory (and autoimmune) activities. If this is the case, long HA may be used for therapy of both malignant and inflammatory diseases. Moreover, targeting the interaction between short HA and CD44 (e.g. by anti-CD44 blocking antibodies) may display also a therapeutic effect on both malignant and inflammatory diseases, an issue that encourages not only fruitful exchange of views, but also practical experimental collaboration.

Autoimmunity --- hyaluronan --- therapy --- hyaluronan synthase --- Inflammation --- Tissue microenvironment --- CD44 --- Cancer