Abstract
Inflammation can occur in response to transient or chronic conditions. Transient inflammation is beneficial during injury or invasion of pathogens. Chronic inflammation presents an unresolved response which can have harmful consequences to the host system. Inflammation is prevalent in multiple human diseases. Current studies provide a strong association between inflammation and cancer. Mitochondrial dysfunction augments the production of mitochondrial reactive oxygen species (mtROS) to support inflammation and proliferation via release of various cytokines. Inflammation, in turn, can further induce mitochondrial dysfunction and reactive oxygen species (ROS) to create a feedback loop of inflammatory insult, which supports the growth and survival of tumor cells. Current pharmacological agents seek to exploit this process by targeting either the mitochondria or downstream targets of the mitochondria which promote inflammation. This chapter delves into the origins of mitochondrial dysfunction and the corresponding signaling pathways that regulate inflammation in cancer.
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This work was supported by the National Cancer Institute (Award Number RO1-CA160685) and the American Cancer Society Research Scholar Grant RSG-12-214-01—CCG to D. Chandra. This work is also supported in part by the National Cancer Institute Center Support Grant P30-CA016056 to the Roswell Park Comprehensive Cancer Center.
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Inigo, J., Woytash, J., Kumar, R., Chandra, D. (2021). Mitochondrial Regulation of Inflammation in Cancer. In: Sun, J. (eds) Inflammation, Infection, and Microbiome in Cancers. Physiology in Health and Disease. Springer, Cham. https://doi.org/10.1007/978-3-030-67951-4_13
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