Oxidative stress, inflammation, and cancer: how are they linked?
Oxidative stress, inflammation, and cancer: how are they linked?
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DOI：
10.1016/j.freeradbiomed.2010.09.006
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发表时间：
2010-12-01
影响因子：
7.4
通讯作者：
Aggarwal, Bharat B.
中科院分区：
文献类型：
--
作者：
Reuter, Simone;Gupta, Subash C.;Chaturvedi, Madan M.;Aggarwal, Bharat B.
过去二十年的广泛研究揭示了持续氧化应激可导致慢性炎症的机制，而慢性炎症又可介导大多数慢性疾病，包括癌症、糖尿病、心血管、神经和肺部疾病。氧化应激可激活多种转录因子，包括NF-κB、AP-1、p53、HIF-1α、PPAR-γ、β-catenin/Wnt和Nrf 2。这些转录因子的激活可导致超过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的基因。氧化应激如何激活炎症通路，导致正常细胞转化为肿瘤细胞，肿瘤细胞的生存，增殖，化疗耐药性，放射抗性，侵袭，血管生成和干细胞存活是本文的重点。总的来说，迄今为止的观察表明，氧化应激，慢性炎症和癌症密切相关。
Extensive research during last two 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, 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.
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