| Xiao Chu,Xinqiang Ji,Mingcui Wang,Wenqing Zhang,Hui Ou,Chong Liu. Up-regulation of Raf kinase inhibitor protein enhances chemosensitivity of cervical cancer cell. Oncol Transl Med, 2014, 13: 101-104. |
| Raf激酶抑制蛋白增强宫颈癌细胞的化疗敏感性 |
| Up-regulation of Raf kinase inhibitor protein enhances chemosensitivity of cervical cancer cell |
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| DOI： |
| 中文关键词: Raf激酶抑制蛋白;Hela细胞;顺铂;化疗敏感性 |
| 英文关键词: Raf kinase inhibitor protein (RKIP); Hela; cisplatin; chemosensitivity |
| 基金项目:青岛市公共领域科技支撑计划项目(No.09-1-1-13-nsh) |
| Author Name | Affiliation | | Xiao Chu | Qingdao University, Qingdao 266003, China | | Xinqiang Ji | Qingdao University, Qingdao 266004, China | | Mingcui Wang | Qingdao University, Qingdao 266005, China | | Wenqing Zhang | Qingdao University, Qingdao 266006, China | | Hui Ou | Qingdao University, Qingdao 266007, China | | Chong Liu | Qingdao University, Qingdao 266008, China |
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| 中文摘要: |
| 目的:探讨Raf激酶抑制蛋白对宫颈癌细胞化疗敏感性的影响。方法:以脂质体法将含有人全长RKIP基因的真核表达质粒pcDNA3.1(+)-ssRKIP转染入宫颈癌Hela细胞中,G418筛选出含目的基因的稳定细胞系,Western blotting法检测Hela细胞中RKIP蛋白的表达。不同浓度顺铂作用不同时间,MTT法观察RKIP转染对顺铂作用于Hela细胞增值的影响,流式细胞术检测RKIP基因转染对顺铂诱导Hela细胞凋亡的影响。结果:pcDNA3.1(+)-ssRKIP转染的Hela细胞RKIP蛋白表达明显升高。不同浓度顺铂分别处理细胞24、48、72 h后,RKIP基因转染的Hela细胞增殖抑制率显著高于对照组细胞(P<0.05)。用5μg/ml顺铂作用Hela细胞24 h后,RKIP转染组的细胞凋亡率为(23.2±0.24)％,明显高于未转染组的(12.4±0.31)％和转染空质粒组的(13.4±0.47)％(P<0.05);在无顺铂作用情况下,RKIP转染组的细胞凋亡率为(5.7±0.12)％,仍然高于未转染组的(2.9±0.21)％和转染空质粒组的(3.6±0.08)％(P<0.05)。结论:RKIP基因表达上调可以增加宫颈癌Hela细胞对化疗药物顺铂的敏感性。 |
| 英文摘要: |
| Objective: The purpose of the study is to investigate the effects of up-regulation of Raf kinase inhibitor protein (RKlP) on the chemosensitivity of cervical cancer Hela cells. Methods: Eukaryotic expression plasmid pcDNA3.1(+)-ssRKIP containing human overall length RKIPcDNA was transfected into cervical cancer Hela cell by lipofectin assay, establishing a stable cell line containing a target gene by G418. Expression of RKIP in Hela cells was measured by Western blot analysis. After treatment with cisplatin of different concentrations and intervals of time, the effect of RKIP on the proliferation of Hela cells was evaluated by MTT method. The flow cytometry was used to investigate whether the RKIP could inhibit apoptosis in Hela cells induced by cisplatin. Results: The expression of RKIP in Hela cells transfected with pcDNA3.1-ssRKIP was increased obviously. After different concentrations of cisplatin treatment cells for 24, 48 and 72 h, the growth inhibition rate in Hela cells transfected with pcDNA3.1-ssRKIP was significantly higher than in control cells (P < 0.05). With 5 μg/mL cisplatin treatment for 24 h, pcDNA3.1-ssRKIP-transfected Hela cells had an obviously higher percentage of apoptosis (23.2 ± 0.24)% than non-transfected cells (12.4 ± 0.31)% and empty vector-transfected cells (13.4 ± 0.47)%. Without treatment of cisplatin, the percentage of apoptosis for Hela cells transfected with pcDNA3.1-ssRKIP was (5.7 ± 0.12)%, which was still higher than those of the non-transfected cells (2.9 ± 0.21)% and empty vector-transfected cells (3 ± 0.08)%. Conclusion: Higher expression of RKIP gene can improve chemosensitivitv of cervical cancer Hela cells to cisplatin. |
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