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PROL4提高肺癌细胞LTEP-a-2对化疗药物顺铂的敏感性
引用本文:何进军,刘传军,刘丹慧,刘吉福,武珊珊,肖雪媛,何大澄.PROL4提高肺癌细胞LTEP-a-2对化疗药物顺铂的敏感性[J].生物化学与生物物理进展,2012,39(9):919-925.
作者姓名:何进军  刘传军  刘丹慧  刘吉福  武珊珊  肖雪媛  何大澄
作者单位:北京师范大学细胞增殖及调控生物学教育部重点实验室;温州医学院浙江省医学遗传学重点实验室;北京军区总院心胸外科
基金项目:国家重点基础研究发展计划(973)(2010CB912203, 2011CB915504, 2011CB710901)和中央高校基本科研业务费专项资金(105566GK)资助项目
摘    要:PROL4(proline-rich protein 4)是我们筛选发现的一个在肺癌细胞中表达缺失的基因.为了深入研究其在肺癌中的生物学功能,构建了PROL4表达质粒,转染肺腺癌LTEP-a-2细胞,获得了稳定表达PROL4的单克隆细胞株.与空载对照细胞相比,过表达PROL4的LTEP-a-2细胞其生长的血清依赖性明显提高,软琼脂集落形成能力降低,裸鼠皮下荷瘤生长受到明显抑制.进一步研究发现,过表达PROL4可明显提高多种肺癌细胞对顺铂的敏感性,而且这种敏感性的提高与PROL4协同顺铂促进细胞凋亡密切相关.该研究结果为临床上如何提高肺癌的化疗效果提供了重要的实验依据.

关 键 词:PROL4,肺癌,顺铂,药物敏感性,凋亡
收稿时间:2011/11/30 0:00:00
修稿时间:2011/12/24 0:00:00

PROL4 Elevates The Sensitivity of Lung Cancer Cell LTEP-a-2 to Cisplatin Treatment
HE Jin-Jun,LIU Chuan-Jun,LIU Dan-Hui,LIU Ji-Fu,WU Shan-Shan,XIAO Xue-Yuan and HE Da-Cheng.PROL4 Elevates The Sensitivity of Lung Cancer Cell LTEP-a-2 to Cisplatin Treatment[J].Progress In Biochemistry and Biophysics,2012,39(9):919-925.
Authors:HE Jin-Jun  LIU Chuan-Jun  LIU Dan-Hui  LIU Ji-Fu  WU Shan-Shan  XIAO Xue-Yuan and HE Da-Cheng
Institution:1)(1) Key Laboratory of Cell Proliferation and Regulation Biology,Ministry of Education,Beijing Normal University,Beijing 100875,China;2) Zhejiang Provincial Key Laboratory of Medical Genetics,Wenzhou Medical College,Wenzhou 325035,China;3) Cardiovascular Surgical of Beijing Military General Hospital,Beijing 100700,China)
Abstract:PROL4 (proline-rich protein 4) was screened out in lung cancer cells for its defective expression in our previous study. By transfection of PROL4 into lung adenocarcinoma cell line LTEP-a-2, a stable cell strain was acquired. It was shown that in PROL4 expressing cells, compared to the vector control cells, the serum dependence of cell growth was markedly enhanced, soft agar colony-forming ability was suppressed. The tumor growth was also significantly restrained by PROL4 in vivo experiments. Furthermore, PROL4 transfected cancer cell strains were found to display an elevated sensitivity to cisplatin treatment than mock-transfectant control cells, and the sensitivity up-regulation was closely related to the rate of cell apoptosis induced by PROL4 and cisplatin cooperately. These results suggest that PROL4 is potentially a new genetic engineering target to enhance the chemotherapeutic effects of cisplatin in lung cancer treatment.
Keywords:PROL4  lung cancer  cisplatin  drug sensitivity  apoptosis
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