辐射致鼻咽癌细胞株cdkl和survivin表达与细胞增殖时相转换的关系  

Expressions of cdkl and survivin by human nasopharyngeal carcinoma cell lines to exposure to irradiation in relation with cell cycle modulation

作　　者：彭涛[1] 袁玉林[2] 张岑[1] 周绪红[1] 

机构地区：[1]武汉大学中南医院耳鼻咽喉一头颈外科 [2]武汉大学基础医学院人体解剖胚胎学教研室,武汉430071

出　　处：《解剖学杂志》2014年第1期18-21,50,F0002,共6页Chinese Journal of Anatomy

基　　金：湖北省自然科学基金（301132174）

摘　　要：目的：探讨鼻咽癌细胞放疗后肿瘤细胞加速衰老及辐射抗拒机制。方法：采用免疫印迹，流式细胞术，sA-β-gal及H-E染色，BrdU细胞标记及细胞计数的方法，检测鼻咽癌CNE2细胞株5Gy间断照射后，细胞周期时相与cdc2／cdkl和survivin蛋白表达的关系。结果：鼻咽癌细胞株射线5Gy间断照射期间及照射后的2～6d内，细胞BrdU标记率大于90％，SA-β-gal阳性细胞小于3％，流式显示G2／M期细胞比例增多，cdkl和survivin表达无明显变化，PCNA表达稍有增加，此期即加速增殖期；细胞处理后第7天～25天，流式显示G1／S期细胞比例增多，BrdU标记率小于10％，SA-β-gal染色阳性细胞达55％以上，H-E染色可见四倍体细胞，cdkl和survivin表达明显下降，PCNA下调不明显，此期即细胞增殖阻滞期；照射细胞后第26天以后，细胞BrdU标记率恢复大于90％，sA-β-gal阳性细胞小于3％，流式检测G2／M期细胞比例增多，cdkl和survivin表达明显上调，此期即再增殖期，结论：细胞衰老可能是人鼻咽癌细胞放射后的反应，衰老细胞中cdkl和survivin表达上调可能是鼻咽癌衰老细胞再增殖机制，也可能是鼻咽癌局部复发和进展的根源。Objective： To investigate the mechanism of accelerated cellular senescence （ACS） and radioresistant in nasopharyngeal carcinoma cell line CNE2 treated-ray. Methods： Western blot, flow cytometry by propidium iodide （PI） staining, BrdU staining, SAβ-gal, hematoxylin and eosin （HE） staining and cell counting detected, respectively, expression of cdc2/cdkl and survivin, cell cycle stages and proliferation and change in cell senescence and morphology. Results： Following exposure to ionizing radiation （IR） with incontinuous 5 Gy for 3 times, CNE2 cell showed a BrdU-labeling index of 90% and the positive for SA-β-Gal of 3%, as well as concomitant cell cycle arrest in G2/M, and no significant change was detected for the cdkl and survivin from 1- 15 days. CNE2 cell showed a BrdUdabeling index of 3% and the positive stain for SA-β-Gal of 55%, as well as concomitant cell cycle arrest in G0/G1, and significant decrease was detected for the cdkl and survivin from 15 to 26 days after IR. CNE2 cell again showed a BrdU-labeling index of 90% and the positive for SAβ-Gal of 3%, as well as concomitant cell cycle arrest in G2/M, and significant increase was detected for the cdkl and survivin from 27 to any days after IR. Conclusion： We propose that ACS is one of the mechanism of in vivo tumor response to irradiation and that mechanisms aberrantly up-regulate Cdkl and survivin promotes escape from the senescence pathway may he involved in a subset of tumors and likely accounts for tumor recurrence/progression.

关 键 词：鼻咽癌 加速衰老 辐射抗拒 

分 类 号：R734.201[医药卫生—肿瘤]