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环氧化酶-2的抑制使肺癌细胞对辐射诱导的凋亡敏感。

Inhibition of cyclooxygenase-2 sensitizes lung cancer cells to radiation-induced apoptosis.

作者信息

Han Zhi-Qiang, Liao Hongwei, Shi Feng, Chen Xiao-Ping, Hu Hua-Cheng, Tian Ming-Qing, Wang Li-Hua, Ying Songmin

机构信息

Department of Respiratory Internal Medicine, People's Hospital of Quzhou City, Quzhou, Zhejiang 324000, P.R. China.

Institute of Respiratory Diseases, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310058, P.R. China.

出版信息

Oncol Lett. 2017 Nov;14(5):5959-5965. doi: 10.3892/ol.2017.6940. Epub 2017 Sep 14.

DOI:10.3892/ol.2017.6940
PMID:29113232
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5661612/
Abstract

Radiotherapy resistance is an enduring major setback in lung cancer therapy, and is responsible for a large proportion of treatment failures. In previous years, cyclooxygenase-2 (COX-2) has frequently been reported to promote tumor occurrence and development, suggesting a potential role in radiotherapy resistance. To investigate whether COX-2 inhibitors can be applied in radiosensitization, an MTT assay was performed to examine cell viability after X-ray radiation in the presence or absence of the specific COX-2 inhibitor Celecoxib. Cell apoptosis and cell cycle changes were also detected through laser confocal scanning microcopy and flow cytometry. X-ray treatment only caused mild cell death in lung cancer A549 cells. However, combination treatment using celecoxib and X-ray radiation exhibited improved inhibitory effects and significantly suppressed cell proliferation. Therefore, COX-2 inhibitors combined with radiotherapy can counteract radiation-induced high COX-2 expression, demonstrating that celecoxib can function as a radiosensitizer of lung cancer cells. It is therefore reasonable to predict COX-2 inhibitors to be potential clinical radiotherapy synergists.

摘要

放疗抵抗是肺癌治疗中一个长期存在的重大障碍,并且是导致很大一部分治疗失败的原因。在过去几年中,经常有报道称环氧合酶-2(COX-2)可促进肿瘤的发生和发展,这表明其在放疗抵抗中可能发挥作用。为了研究COX-2抑制剂是否可用于放射增敏,进行了MTT试验,以检测在存在或不存在特异性COX-2抑制剂塞来昔布的情况下,X射线辐射后细胞的活力。还通过激光共聚焦扫描显微镜和流式细胞术检测了细胞凋亡和细胞周期变化。X射线处理仅在肺癌A549细胞中引起轻度细胞死亡。然而,塞来昔布与X射线辐射联合治疗表现出更好的抑制效果,并显著抑制细胞增殖。因此,COX-2抑制剂与放疗联合可抵消辐射诱导的COX-2高表达,这表明塞来昔布可作为肺癌细胞的放射增敏剂。因此,预测COX-2抑制剂为潜在的临床放疗增效剂是合理的。

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本文引用的文献

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Reduction in cancer risk by selective and nonselective cyclooxygenase-2 (COX-2) inhibitors.选择性和非选择性环氧化酶-2(COX-2)抑制剂对癌症风险的降低作用。
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Celecoxib enhances the sensitivity of non-small-cell lung cancer cells to radiation-induced apoptosis through downregulation of the Akt/mTOR signaling pathway and COX-2 expression.塞来昔布通过下调 Akt/mTOR 信号通路和 COX-2 表达增强非小细胞肺癌细胞对放射诱导凋亡的敏感性。
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