Abstract
Both oxidative stress and inflammation are interdependent cellular consequences of a biological defense system, which can fuel cancer and other pathophysiological provenience. In recent past, several emerging evidences showed that prevalence of oxidative stress and inflammation promotes multiple oncogenic events, including cell proliferation, angiogenesis, migration, metabolic reprogramming, and evasion of regulated cell death in cancer cells. Oxidative stress and chronic inflammation contribute to the progression of cancer in a unanimous pattern with significant cellular signaling response and outcomes. However, both oxidative stress and inflammation are also associated with the pathogenesis of several other diseases. The oxidative stress is an imbalance between oxidant and antioxidant defense system, which in turn damaging the macromolecules and dysregulation of complex casacde of cell signaling. Sustained oxidative stress can trigger chronic inflammation by activating the number of transcription factors such as NF-κB, AP-1, β-catenin/Wnt, p53, PPAR-γ, HIF-1α, and Nrf2. The activation of these transcription factors leads to altered expression of various genes and proteins including growth factors, cell cycle regulatory molecules, oncogenes, tumor suppressor genes, pro-inflammatory cytokines, and chemokines etc. Reprogramming of the cellular signaling cascade for self-survival is one of the key characteristics of cancer cells. In this chapter, we delineate the current knowledge and mechanistic interplay between oxidative stress and inflammation, which can fuel cancer.
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Vaidya, F.U., Chhipa, A.S., Sagar, N., Pathak, C. (2020). Oxidative Stress and Inflammation Can Fuel Cancer. In: Maurya, P., Dua, K. (eds) Role of Oxidative Stress in Pathophysiology of Diseases. Springer, Singapore. https://doi.org/10.1007/978-981-15-1568-2_14
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