IKK/NF-κB signaling: balancing life and death – a new approach to cancer therapy
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TLDR
Inhibition of IKK-driven NF-kappaB activation offers a strategy for treatment of different malignancies and can convert inflammation- induced tumor growth to inflammation-induced tumor regression.Abstract:
IkappaB kinase/NF-kappaB (IKK/NF-kappaB) signaling pathways play critical roles in a variety of physiological and pathological processes. One function of NF-kappaB is promotion of cell survival through induction of target genes, whose products inhibit components of the apoptotic machinery in normal and cancerous cells. NF-kappaB can also prevent programmed necrosis by inducing genes encoding antioxidant proteins. Regardless of mechanism, many cancer cells, of either epithelial or hematopoietic origin, use NF-kappaB to achieve resistance to anticancer drugs, radiation, and death cytokines. Hence, inhibition of IKK-driven NF-kappaB activation offers a strategy for treatment of different malignancies and can convert inflammation-induced tumor growth to inflammation-induced tumor regression.read more
Citations
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Journal ArticleDOI
Integrating cell-signalling pathways with NF-kappaB and IKK function.
TL;DR: This work has shown that crosstalk constitutes a decision-making process that determines the consequences of NF-κB and IKK activation and, ultimately, cell fate.
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A cytokine-mediated link between innate immunity, inflammation, and cancer
Wan-Wan Lin,Michael Karin +1 more
TL;DR: An overview of the current understanding of the role of inflammation-induced cytokines in tumor initiation, promotion, and progression is provided.
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NF-κB, inflammation, immunity and cancer: coming of age
Koji Taniguchi,Michael Karin +1 more
TL;DR: How the initial discovery of a role for NF-κB in linking inflammation and cancer led to an improved understanding of tumour-elicited inflammation and its effects on anticancer immunity is discussed.
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An Epigenetic Switch Involving NF-κB, Lin28, Let-7 MicroRNA, and IL6 Links Inflammation to Cell Transformation
TL;DR: It is shown that transient activation of Src oncoprotein can mediate an epigenetic switch from immortalized breast cells to a stably transformed line that forms self-renewing mammospheres that contain cancer stem cells.
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Mechanisms of cell death in oxidative stress.
Stefan W. Ryter,Hong Pyo Kim,Alexander Hoetzel,Jeong W. Park,Kiichi Nakahira,Xue Wang,Augustine M.K. Choi +6 more
TL;DR: Cell death mechanisms have been studied across a broad spectrum of models of oxidative stress, including H2O2, nitric oxide and derivatives, endotoxin-induced inflammation, photodynamic therapy, ultraviolet-A and ionizing radiations, and cigarette smoke.
References
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