摘要
有研究证明电离辐射激活转录因子,从而引起治疗癌细胞的抵抗。这与激活促生存前信号通路和导致癌症发生发展有关。在不刺激的情况下,转录因子NF-κB是被隔离在细胞质中的,但是当细胞被电离辐射后,蛋白酶体通过IKK中IκB流动磷酸化蛋白酶降解,异常地导致NF-κB激活和核转位。因此,IκB降解、蛋白酶体作用、IKK磷酸蛋白酶和NF-κB核转位的干扰为抑制电离辐射诱导的NF-κB的副作用提供了坚定的策略。尽管NF-κB分子机制没有得到完整的解析,为了抑制由电离辐射引起的NF-κB,不同NF-κB抑制剂已经被使用。本文旨在强调电离辐射介导的NF-κB,如MG132、硼替佐米、姜黄色素、DHMEQ、橙皮苷、索拉菲尼以及银胶菊内酯在抑制电离辐射诱导的NF-κB副作用中的作用。此外也讨论了它们的化学结构特征和分子机制。
关键词: 转录因子;肿瘤;辐射增敏;辐射保护;辐射;NF-κB抑制剂
Current Medicinal Chemistry
Title:The Role of NF-κB Inhibitors in Cell Response to Radiation
Volume: 23 Issue: 34
Author(s): Sajjad Molavi Pordanjani, Seyed Jalal Hosseinimehr
Affiliation:
关键词: 转录因子;肿瘤;辐射增敏;辐射保护;辐射;NF-κB抑制剂
摘要: 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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Cite this article as:
Sajjad Molavi Pordanjani, Seyed Jalal Hosseinimehr , The Role of NF-κB Inhibitors in Cell Response to Radiation, Current Medicinal Chemistry 2016; 23 (34) . https://dx.doi.org/10.2174/0929867323666160824162718
DOI https://dx.doi.org/10.2174/0929867323666160824162718 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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