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2000
Volume 23, Issue 34
  • ISSN: 0929-8673
  • E-ISSN: 1875-533X

Abstract

It is well documented that ionizing radiation (IR) activates the transcription factor (NF-κB) which is a trigger for resistance cancer cells to treatment. It is involved in activation of pro-survival signaling pathways and resulting in cancer development and progression. In unstimulated condition, NF-κB is sequestered in cytoplasm but after the cell exposure to IR, proteasomal degradation of IΚB flowing phosphorylation via IKK, leads to aberrantly NF-κB activation and nuclear translocation. Therefore, interruption in IΚB degradation, proteasome action, IKK phosphorylation and NF-κB nuclear translocation provide robust strategies for inhibiting adverse effect of IR induced NF-κB. In spite of uncompleted elucidation of NF-κB molecular mechanisms, different NF-κB inhibitors have been used in order to inhibiting the IR induced NF-κB. The aim of this review is to highlight the role of IR induced-NF-κB inhibitors such as MG132, bortezomib, curcumin, DHMEQ, naringin, sorafenib, genistein and parthenolide in suppression of IR induced NF-κB adverse effects. Moreover, their chemical, structural characteristics and molecular mechanisms will be discussed.

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/content/journals/cmc/10.2174/0929867323666160824162718
2016-10-01
2025-01-30
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  • Article Type:
    Research Article
Keyword(s): NF-ΚB inhibitors; radiation; radioprotective; radiosensitizing; Transcription factor; tumor
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