Halofuginone enhances the radiation sensitivity of human tumor cell lines

被引：19

作者：

Cook, John A. ^{[1
]}

Choudhuri, Rajani ^{[1
]}

DeGraff, William ^{[1
]}

Gamson, Janet ^{[1
]}

Mitchell, James B. ^{[1
]}

机构：

[1] NCI, Radiat Biol Branch, Ctr Canc Res, Bethesda, MD 20892 USA

来源：

CANCER LETTERS | 2010年 / 289卷 / 01期

关键词：

Radiation sensitizer; TGF-beta; Halofuginone; Fibrosis; TGF-BETA; HEPATOCELLULAR-CARCINOMA; H2AX PHOSPHORYLATION; HISTONE H2AX; CANCER CELLS; DNA-DAMAGE; GROWTH; INHIBITION; THERAPY; INJURY;

D O I：

10.1016/j.canlet.2009.08.009

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

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 TGE-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 TGE-beta pathway to achieve a positive increase in the therapeutic gain in clinical radiotherapy. Published by Elsevier Ireland Ltd.

引用

页码：119 / 126

页数：8

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