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Journal ArticleDOI

Nuclear factor-κB inhibitors as sensitizers to anticancer drugs

Chikashi Nakanishi, +1 more
- 01 Apr 2005 - 
- Vol. 5, Iss: 4, pp 297-309
TLDR
The cytotoxicity of chemotherapeutic agents is attributed to apoptosis, and there is evidence that inhibitors of NF-κB might promote apoptosis in cancer cells and can NF-σB inhibitors be used to overcome resistance to chemotherAPEutic agents.
Abstract
The cytotoxicity of chemotherapeutic agents is attributed to apoptosis. Acquired resistance to the effects of chemotherapy has emerged as a significant impediment to effective cancer therapy. One feature that cytotoxic treatments of cancer have in common is their activation of the transcription factor nuclear factor-kappaB (NF-kappaB), which regulates cell survival. NF-kappaB activation suppresses the apoptotic potential of chemotherapeutic agents and contributes to resistance. What evidence is there that inhibitors of NF-kappaB might promote apoptosis in cancer cells and can NF-kappaB inhibitors be used to overcome resistance to chemotherapeutic agents?

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Citations
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Molecular mechanisms of necroptosis: an ordered cellular explosion.

TL;DR: Evidence now reveals that necrosis can also occur in a regulated manner, and necroptosis participates in the pathogenesis of diseases, including ischaemic injury, neurodegeneration and viral infection, thereby representing an attractive target for the avoidance of unwarranted cell death.
Journal ArticleDOI

Inflammation meets cancer, with NF-κB as the matchmaker

TL;DR: Although it seems to fulfill a distinctly tumor-promoting role in many types of cancer, NF-κB has a confounding role in certain tumors.
Journal ArticleDOI

Is NF-κB a good target for cancer therapy? Hopes and pitfalls

TL;DR: Recent evidence from cancer genetics and cancer genome studies that support the involvement of NF-κB in human cancer, particularly in multiple myeloma are discussed.
Journal ArticleDOI

Strategies to improve radiotherapy with targeted drugs

TL;DR: Improved understanding of the molecular response of cells and tissues to ionizing radiation and a new appreciation of the exploitable genetic alterations in tumours have led to the development of treatments combining pharmacological interventions with ionizing Radiation that more specifically target either tumour or normal tissue, leading to improvements in efficacy.
Journal ArticleDOI

Discovery and Development of the G-rich Oligonucleotide AS1411 as a Novel Treatment for Cancer

TL;DR: The serendipitous discovery of the G-rich oligonucleotides led to the identification of nucleolin as a new molecular target for cancer therapy, and this molecule functions as an aptamer to nucleolin, a multifunctional protein that is highly expressed by cancer cells, both intracellularly and on the cell surface.
References
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Journal ArticleDOI

Phosphorylation meets ubiquitination: the control of NF-[kappa]B activity.

TL;DR: Recent progress has been made in understanding the details of the signaling pathways that regulate NF-kappaB activity, particularly those responding to the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1.
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Signaling to NF-kappaB.

TL;DR: An overview of established NF-kappaB signaling pathways is provided with focus on the current state of research into the mechanisms that regulate IKK activation and NF- kappaB transcriptional activity.
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TNF- and Cancer Therapy-Induced Apoptosis: Potentiation by Inhibition of NF-κB

TL;DR: The activation of the transcription factor nuclear factor-kappa B by tumor necrosis factor, ionizing radiation, or daunorubicin, was found to protect from cell killing, providing a mechanism of cellular resistance to killing by some apoptotic reagents.
Journal ArticleDOI

IAP family proteins—suppressors of apoptosis

TL;DR: Although the mechanism used by the IAPs to suppress cell death remains debated, several studies have provided insights into the biochemical functions of these intriguing proteins and a variety of reports have suggested an important role for the I APs in some human diseases.
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