Cholesterol and Radiosensitivity
Cholesterol and Radiosensitivity
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胆固醇和放射敏感性
DOI：
10.1007/s12609-016-0202-y
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发表时间：
2016
影响因子：
0.9
通讯作者：
W. Woodward
中科院分区：
文献类型：
--
作者：
Omar M. Rahal;W. Woodward
虽然在动物研究中有一些证据表明胆固醇信号介导了正常组织的辐射敏感性，但直到最近，还没有发现胆固醇信号与肿瘤放射敏感性之间的联系。乳腺癌中异常的胆固醇信号通过改变膜流动性、膜相关筏或作为直接转录激活因子促进肿瘤发生和肿瘤进展。胆固醇是通过甲氧戊酸途径重新合成的。羟基-3-甲基戊二酰辅酶A还原酶是甲氧戊酸途径的限速酶，在肿瘤转化、进展和治疗敏感性中的因果作用为抑制该酶的药物(即他汀类药物)以及其他胆固醇调节策略提供了放射增敏治疗的机会。这篇综述讨论了他汀类药物改变乳腺癌中胆固醇信号的潜在机制，并特别关注炎症性乳腺癌，潜在地增强了辐射敏感性和预后。
Although there is some evidence in animal studies that cholesterol signaling mediates radiation sensitivity of normal tissues, until recently, no connection had been made between cholesterol signaling and tumor radiosensitivity. Aberrant cholesterol signaling in breast cancer promotes oncogenesis and tumor progression by either altering membrane fluidity, membrane associated rafts, or as a direct activator of transcription. Cholesterol is synthesized de novo by the mevalonate pathway. A causal role for hydroxy-3-methylglutaryl-coenzyme A reductase, a rate-limiting enzyme of the mevalonate pathway, in oncogenic transformation, progression, and sensitivity to treatment offers an opportunity for drugs that inhibit this enzyme (i.e., statins) as well as other cholesterol mediating strategies as radiosensitizing treatments. This review discusses potential mechanisms by which statins alter cholesterol signaling in breast cancer and potentially enhances radiation sensitivity and outcome with a special focus on inflammatory breast cancer.
影响因子：
10.5
作者：
Dontu, G;Abdallah, WM;Wicha, MS
通讯作者：
Wicha, MS