2010 December 1; 49(11): 1603–1616. | Simone Reuter, Subash C. Gupta, Madan M. Chaturvedi, and Bharat B. Aggarwal
The article reviews the link between oxidative stress, inflammation, and cancer. Oxidative stress, defined as an imbalance between the production of reactive oxygen species (ROS) and their elimination by antioxidants, can activate various transcription factors such as NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. These transcription factors can lead to the expression of over 500 genes involved in growth, inflammation, and cell cycle regulation. Chronic inflammation, induced by various factors, is associated with an increased risk of cancer. The review discusses how oxidative stress activates inflammatory pathways, leading to cellular transformation, survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival. It highlights the role of ROS in damaging DNA, promoting genomic instability, and activating signaling pathways that support tumor development. The article also explores the involvement of ROS in the inflammatory tumor microenvironment, which modulates cancer development and resistance to anticancer therapies. Overall, the evidence suggests a close link between oxidative stress, chronic inflammation, and cancer.The article reviews the link between oxidative stress, inflammation, and cancer. Oxidative stress, defined as an imbalance between the production of reactive oxygen species (ROS) and their elimination by antioxidants, can activate various transcription factors such as NF-κB, AP-1, p53, HIF-1α, PPAR-γ, β-catenin/Wnt, and Nrf2. These transcription factors can lead to the expression of over 500 genes involved in growth, inflammation, and cell cycle regulation. Chronic inflammation, induced by various factors, is associated with an increased risk of cancer. The review discusses how oxidative stress activates inflammatory pathways, leading to cellular transformation, survival, proliferation, chemoresistance, radioresistance, invasion, angiogenesis, and stem cell survival. It highlights the role of ROS in damaging DNA, promoting genomic instability, and activating signaling pathways that support tumor development. The article also explores the involvement of ROS in the inflammatory tumor microenvironment, which modulates cancer development and resistance to anticancer therapies. Overall, the evidence suggests a close link between oxidative stress, chronic inflammation, and cancer.