Department of Biological and Chemical Sciences, New York Institute of Technology, New York, NY, United States.
Department of Molecular, Cellular and Biomedical Sciences, Sophie Davis School of Biomedical Education, City University of New York School of Medicine, New York, NY, United States; Graduate Program in Biology, City University of New York Graduate Center, New York, NY, United States.
Biochem Pharmacol. 2020 Jun;176:113899. doi: 10.1016/j.bcp.2020.113899. Epub 2020 Mar 4.
Nitric oxide (NO) and its pro and anti-tumor activities are dual roles that continue to be debated in cancer biology. The cell situations in the tumor and within the tumor microenvironment also have roles involving NO. In early tumorigenic events, macrophages in the tumor microenvironment promote tumor cell death, and later are reprogramed to support the growth of tumor, through regulatory events involving NO and several stimulatory signals. These two opposing and active phenotypes of tumor associated macrophages known as the M1 or anti-tumorigenic state and M2 or pro-tumorigenic state show differences in metabolic pathways such as glycolysis and arginine utilization, signaling pathways and cytokine induction including iNOS expression, therefore contributing to their function. Polarization of M2 to M1 macrophages, inhibition of M2 state, or reprogramming via NO in combination with other signals may determine or alter tumor kinetics. These strategies and an overview are presented.
一氧化氮（NO）及其抗肿瘤活性具有双重作用，这在癌症生物学中仍存在争议。肿瘤细胞和肿瘤微环境中的细胞情况也涉及到 NO。在早期肿瘤发生事件中，肿瘤微环境中的巨噬细胞促进肿瘤细胞死亡，后来通过涉及 NO 和几种刺激信号的调节事件被重新编程以支持肿瘤的生长。这两种对立且活跃的肿瘤相关巨噬细胞表型被称为 M1 或抗肿瘤状态和 M2 或促肿瘤状态，它们在代谢途径（如糖酵解和精氨酸利用）、信号通路和细胞因子诱导（包括 iNOS 表达）方面存在差异，因此对其功能有贡献。M2 向 M1 巨噬细胞的极化、M2 状态的抑制或通过与其他信号结合的 NO 进行重编程可能决定或改变肿瘤动力学。本文介绍了这些策略和概述。
