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首页> 外文期刊>Nitric oxide: Biology and chemistry >Nitric oxide and interactions with reactive oxygen species in the development of melanoma, breast, and colon cancer: A redox signaling perspective
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Nitric oxide and interactions with reactive oxygen species in the development of melanoma, breast, and colon cancer: A redox signaling perspective

机译：在黑素瘤，乳腺癌和结肠癌发育中的一氧化氮和与反应性氧物种的相互作用：氧化还原信令视角

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摘要

Cancer development is closely related to chronic inflammation, which is associated with identifiable markers of tumor progression, such as uncontrolled cell proliferation, angiogenesis, genomic instability, chemotherapeutic resistance, and metastases. Redox processes mediated by reactive oxygen species (ROS) and nitric oxide (NO) within the inflammatory tumor microenvironment play an essential role in directly influencing intercellular and intracellular signaling. These reactive species originating in the cancer cell or its microenvironment, mediate the epithelial-mesenchymal transition (EMT) and the mesenchymal-epithelial transition (MET). However, intracellular interactions between NO and ROS must be controlled to prevent cell death. Melanoma, breast, and colon cancer cells have developed a mechanism to survive and adapt to oxidative and nitrosative stress. The mechanism involves a spatial-temporal fine adjustment of the intracellular concentrations of NO and ROS, thereby guaranteeing the successful development of cancer cells. Physiological concentrations of NO and supra physiological concentrations of ROS are prevalent in cancer cells at the primary site. The situation reverses in cancer cells undergoing the EMT prior to being released into the blood stream. Intracellular supra physiological concentrations of NO found in circulating cancer cells endow them with anoikis resistance. When the anoikis-resistant cancer cells arrive at a metastatic site they undergo the MET. Endogenous supra physiological concentrations of ROS and physiological NO concentrations are prevalent in these cells. Understanding tumor progression from the perspective of redox signaling permits the characterization of new markers and approaches to therapy. The synthesis and use of compounds with the capacity of modifying intracellular concentrations of NO and ROS may prove effective in disrupting a redox homeostasis operative in cancer cells.
机译：癌症的发展与慢性炎症密切相关，慢性炎症与肿瘤进展的可识别标记相关，例如不受控制的细胞增殖，血管生成，基因组不稳定性，化学治疗性和转移。在炎性肿瘤微环境中由反应性氧物质（ROS）和一氧化氮（NO）介导的氧化还原过程在直接影响细胞间和细胞内信号传导中起重要作用。这些源自癌细胞或其微环境的这些反应性物种介导上皮 - 间充质转换（EMT）和间充质上皮过渡（MET）。然而，必须控制NO和RO之间的细胞内相互作用以防止细胞死亡。黑色素瘤，乳腺和结肠癌细胞已开发出存活并适应氧化和氮化应激的机制。该机制涉及不含NO和RO的细胞内浓度的空间颞次微调，从而保证癌细胞的成功发展。 ROS的NO和SUPRA生理浓度的生理浓度在初级部位的癌细胞中普遍存在。在释放到血液流之前，情况逆转在EMT的癌细胞中逆转。在循环癌细胞中发现的NO细胞内的Supra生理浓度赋予它们抗Anoikis抗性。当抗抗癌的癌细胞到达它们经历的转移部位时。在这些细胞中，内源性的ROS和生理学无浓度的生理浓度普遍存在。理解氧化还原信号传导的角度肿瘤进展允许表征新标记和治疗方法。具有改性NO和RO的细胞内浓度的能量的合成和使用可能有效地破坏癌细胞中的氧化还原性稳态。

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