Nitric oxide and thyroid carcinoma: A review

Figures

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  Figure 1. Function of NO in cancer. NO has dual properties on tumor cells. At low concentration, NO promotes tumor growth and proliferation through GMP-dependent pathway and angiogenesis. At high concentration, NO destroys the DNA of tumor cells by releasing active nitrogen, thus achieving the purpose of inhibiting tumor cells. Furthermore, NO can also accumulate P53 to affect the physiological processes of tumor cells. nNOS, neuronal nitric oxide synthase; eNOS, Endothelial Nitric Oxide Synthase; iNOS, Inducible Nitric Oxide Synthase; NO, nitrous oxide; sGC, Soluble guanylate cyclase; GTP, Guanosine Triphosphate; cGMP, cyclic guanosine monophosphate; VS, versus; VEGF, Vascular Endothelial Growth Factor; HIF1A, Hypoxia inducible factor-1α; DNA, deoxyribonucleic acid; NFkB, nuclear factor κB; ONOO, peroxynitrite anion.

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  Figure 2. Function of NO in thyroid carcinoma The expressions of eNOS and iNOS in thyroid carcinoma tissues are higher than those in normal thyroid tissues. As a result, this increases the content of NO, which promotes tumor growth by regulating angiogenesis and VEGE. When NO is targeted to the thyroid tissue and maintained in high concentration, it can inhibit the growth and proliferation of thyroid tumors and therefore achieve therapeutic goals. NO, nitrous oxide; NOS, Nitric Oxide Synthase; eNOS, Endothelial Nitric Oxide Synthase; iNOS, Inducible Nitric Oxide Synthase; VEGF, Vascular Endothelial Growth Factor.