Key result
iNOS plays a context-dependent dual role in tumor development, exerting both pro- and antitumor effects.
Highlights that iNOS-derived nitric oxide plays a complex, dual role in cancer progression, acting as either a tumor promoter or suppressor depending on the microenvironment and NO concentration.
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iNOS dual roles advise against non-specific inhibition in tumors; leaves open context-specific trials before clinical adoption.
Nitric oxide (NO) is one of the 10 smallest molecules found in nature. It is a simple gaseous free radical whose predominant functions is that of a messenger through cGMP. In mammals, NO is synthesized by the enzyme nitric oxide synthase (NOS) of which there are three isoforms. Neuronal (nNOS, NOS1) and endothelial (eNOS, NOS3) are constitutive calcium-dependent forms of the enzyme that regulate neural and vascular function respectively. The third isoform (iNOS, NOS2), is calcium-independent and is inducible. In many tumors, iNOS expression is high, however, the role of iNOS during tumor development is very complex and quite perplexing, with both promoting and inhibiting actions having been described. This review will aim to summarize the dual actions of iNOS-derived NO showing that the microenvironment of the tumor is a contributing factor to these observations and ultimately to cellular outcomes.
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Vannini et al. (2015) conducted a review in Cancer. iNOS expression (Nitric Oxide production) was evaluated. iNOS has a highly complex and environment-dependent dual role in tumor development, with both tumor-promoting and inhibiting actions depending on cellular context and NO concentration.
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