Division of Endocrinology and Metabolism at Charles Drew University of Medicine and Science, Los Angeles, California 90059, USA.
Curr Pharm Des. 2010;16(4):451-62. doi: 10.2174/138161210790232130.
Nitric oxide is a pleiotropic ancestral molecule, which elicits beneficial effect in many physiological settings but is also tenaciously expressed in numerous pathological conditions, particularly breast tumors. Nitric oxide is particularly harmful in adipogenic milieu of the breast, where it initiates and promotes tumorigenesis. Epidemiological studies have associated populations at a greater risk for developing breast cancer, predominantly estrogen receptor positive tumors, to express specific polymorphic forms of endothelial nitric oxide synthase, that produce sustained low levels of nitric oxide. Low sustained nitric oxide generates oxidative stress and inflammatory conditions at susceptible sites in the heterogeneous microenvironment of the breast, where it promotes cancer related events in specific cell types. Inflammatory conditions also stimulate inducible nitric oxide synthase expression, which dependent on the microenvironment, could promote or inhibit mammary tumors. In this review we re-examine the mechanisms by which nitric oxide promotes initiation and progression of breast cancer and address some of the controversies in the field.
一氧化氮是一种多效的古老分子,在许多生理环境中产生有益的影响,但也顽强地表达在许多病理条件下,特别是乳腺肿瘤。一氧化氮在乳腺的脂肪生成环境中特别有害,它在那里引发并促进肿瘤发生。流行病学研究将罹患乳腺癌风险较高的人群,主要是雌激素受体阳性肿瘤,与表达特定的内皮型一氧化氮合酶的多态形式联系起来,这些形式产生持续的低水平的一氧化氮。低水平的持续一氧化氮会在乳腺异质微环境中的易感部位产生氧化应激和炎症,从而促进特定细胞类型的癌症相关事件。炎症条件也会刺激诱导型一氧化氮合酶的表达,这取决于微环境,可能促进或抑制乳腺肿瘤。在这篇综述中,我们重新审视了一氧化氮促进乳腺癌发生和发展的机制,并解决了该领域的一些争议。