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卤夫酮增强人肿瘤细胞系的辐射敏感性。

Halofuginone enhances the radiation sensitivity of human tumor cell lines.

机构信息

Radiation Biology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD 20892-1002, USA.

出版信息

Cancer Lett. 2010 Mar 1;289(1):119-26. doi: 10.1016/j.canlet.2009.08.009. Epub 2009 Aug 26.

DOI:10.1016/j.canlet.2009.08.009
PMID:19713035
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2835928/
Abstract

Transforming growth factor beta (TGF-beta) is implicated in radiation-induced fibrosis of normal tissues in patients receiving radiotherapy. Inhibiting the TGF-beta signaling pathway by various means has been shown to reduce radiation-induced fibrosis in pre-clinical studies. The present study evaluated the effects of interfering with the TGF-beta signaling pathway on the radiosensitivity of selected human tumor cell lines using the plant-derived alkaloid, halofuginone. Halofuginone treatment inhibited cell growth, halted cell cycle progression, decreased radiation-induced DNA damage repair, and decreased TGF-beta receptor II protein levels, leading to increased cellular radiosensitization. These data further support the goal of manipulating the TGF-beta pathway to achieve a positive increase in the therapeutic gain in clinical radiotherapy.

摘要

转化生长因子-β（TGF-β）与接受放射治疗的患者正常组织的放射性纤维化有关。通过各种手段抑制 TGF-β信号通路已被证明可减少临床前研究中的放射性纤维化。本研究使用植物衍生的生物碱血根碱评估了干扰 TGF-β信号通路对选定的人类肿瘤细胞系放射敏感性的影响。血根碱处理抑制细胞生长、阻止细胞周期进程、减少辐射诱导的 DNA 损伤修复、降低 TGF-β受体 II 蛋白水平，导致细胞放射敏感性增加。这些数据进一步支持操纵 TGF-β途径以在临床放射治疗中实现治疗增益的积极增加的目标。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/7c0ea657cea8/nihms182101f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/7ca64393f03d/nihms182101f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/45510559fc6e/nihms182101f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/166e5790ce69/nihms182101f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/39bc7c76d5d5/nihms182101f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/7c0ea657cea8/nihms182101f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/7ca64393f03d/nihms182101f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/45510559fc6e/nihms182101f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/166e5790ce69/nihms182101f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/39bc7c76d5d5/nihms182101f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7de4/2835928/7c0ea657cea8/nihms182101f5.jpg

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本文引用的文献

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Targeting TGFβ signaling to inhibit fibroblast activation as a therapy for fibrosis and cancer: effect of halofuginone.靶向 TGFβ 信号抑制成纤维细胞活化作为纤维化和癌症的治疗方法：卤夫酮的作用。
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New rationales for using TGFbeta inhibitors in radiotherapy.放疗中使用转化生长因子β抑制剂的新理论依据。
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Phase I and pharmacokinetic study of halofuginone, an oral quinazolinone derivative in patients with advanced solid tumours.卤夫酮（一种口服喹唑啉酮衍生物）在晚期实体瘤患者中的I期和药代动力学研究。
Eur J Cancer. 2006 Aug;42(12):1768-74. doi: 10.1016/j.ejca.2005.12.027. Epub 2006 Jul 3.
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H2AX phosphorylation within the G1 phase after UV irradiation depends on nucleotide excision repair and not DNA double-strand breaks.紫外线照射后G1期内的H2AX磷酸化取决于核苷酸切除修复而非DNA双链断裂。
Proc Natl Acad Sci U S A. 2006 Jun 27;103(26):9891-6. doi: 10.1073/pnas.0603779103. Epub 2006 Jun 20.