Department of Toxicology, Shanxi Provincial Key Lab of Free Radical Biology and Medicine, Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an, 710032 Shaanxi, China.
Department of Occupational & Environmental Health and the Ministry of Education Key Lab of Hazard Assessment and Control in Special Operational Environment, School of Public Health, Fourth Military Medical University, Xi'an 710032, China.
Oxid Med Cell Longev. 2022 Jun 28;2022:2606928. doi: 10.1155/2022/2606928. eCollection 2022.
According to numerous animal studies, adverse environmental stimuli, including physical, chemical, and biological factors, can cause low-grade chronic inflammation and subsequent tumor development. Human epidemiological evidence has confirmed the close relationship between chronic inflammation and tumorigenesis. However, the mechanisms driving the development of persistent inflammation toward tumorigenesis remain unclear. In this study, we assess the potential role of reactive oxygen species (ROS) and associated mechanisms in modulating inflammation-induced tumorigenesis. Recent reports have emphasized the cross-talk between oxidative stress and inflammation in many pathological processes. Exposure to carcinogenic environmental hazards may lead to oxidative damage, which further stimulates the infiltration of various types of inflammatory cells. In turn, increased cytokine and chemokine release from inflammatory cells promotes ROS production in chronic lesions, even in the absence of hazardous stimuli. Moreover, ROS not only cause DNA damage but also participate in cell proliferation, differentiation, and apoptosis by modulating several transcription factors and signaling pathways. We summarize how changes in the redox state can trigger the development of chronic inflammatory lesions into tumors. Generally, cancer cells require an appropriate inflammatory microenvironment to support their growth, spread, and metastasis, and ROS may provide the necessary catalyst for inflammation-driven cancer. In conclusion, ROS bridge the gap between chronic inflammation and tumor development; therefore, targeting ROS and inflammation represents a new avenue for the prevention and treatment of cancer.
根据大量动物研究，包括物理、化学和生物因素在内的不利环境刺激会导致低度慢性炎症和随后的肿瘤发展。人类流行病学证据已经证实了慢性炎症与肿瘤发生之间的密切关系。然而，导致持续炎症向肿瘤发展的机制尚不清楚。在本研究中，我们评估了活性氧（ROS）及其相关机制在调节炎症诱导的肿瘤发生中的潜在作用。最近的报告强调了氧化应激和炎症在许多病理过程中的相互作用。暴露于致癌的环境危害可能导致氧化损伤，这进一步刺激各种类型的炎性细胞浸润。反过来，炎性细胞释放的细胞因子和趋化因子增加会促进慢性病变中的 ROS 产生，即使没有危险刺激也是如此。此外，ROS 不仅会导致 DNA 损伤，还可以通过调节几种转录因子和信号通路来参与细胞增殖、分化和凋亡。我们总结了氧化还原状态的变化如何引发慢性炎症性病变发展为肿瘤。一般来说，癌细胞需要适当的炎症微环境来支持其生长、扩散和转移，而 ROS 可能为炎症驱动的癌症提供必要的催化剂。总之，ROS 弥合了慢性炎症和肿瘤发展之间的差距；因此，靶向 ROS 和炎症代表了预防和治疗癌症的新途径。
