Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Free Radic Biol Med. 2010 Dec 1;49(11):1603-16. doi: 10.1016/j.freeradbiomed.2010.09.006. Epub 2010 Sep 16.
Extensive research during the past 2 decades has revealed the mechanism by which continued oxidative stress can lead to chronic inflammation, which in turn could mediate most chronic diseases including cancer, diabetes, and cardiovascular, neurological, and pulmonary diseases. Oxidative stress can activate a variety of transcription factors including NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. Activation of these transcription factors can lead to the expression of over 500 different genes, including those for growth factors, inflammatory cytokines, chemokines, cell cycle regulatory molecules, and anti-inflammatory molecules. How oxidative stress activates inflammatory pathways leading to transformation of a normal cell to tumor cell, tumor cell survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival is the focus of this review. Overall, observations to date suggest that oxidative stress, chronic inflammation, and cancer are closely linked.
在过去的 20 年中，广泛的研究揭示了持续的氧化应激如何导致慢性炎症，而慢性炎症反过来又可能介导大多数慢性疾病，包括癌症、糖尿病以及心血管、神经和肺部疾病。氧化应激可以激活多种转录因子，包括 NF-κB、AP-1、p53、HIF-1α、PPAR-γ、β-连环蛋白/Wnt 和 Nrf2。这些转录因子的激活可以导致超过 500 种不同基因的表达，包括生长因子、炎性细胞因子、趋化因子、细胞周期调节分子和抗炎分子。氧化应激如何激活炎症途径，导致正常细胞向肿瘤细胞转化、肿瘤细胞存活、增殖、化疗耐药、放疗耐药、侵袭、血管生成和干细胞存活，是本综述的重点。总的来说，迄今为止的观察结果表明，氧化应激、慢性炎症和癌症密切相关。
