白细胞介素37对宫颈癌HeLa细胞顺铂化疗敏感性的增强作用
发布时间：2018-11-17 09:23
【摘要】：目的:通过将白细胞介素37(IL-37)基因转染到宫颈癌HeLa细胞中,探讨IL-37对宫颈癌细胞的杀伤作用及其对宫颈癌细胞化疗敏感性的增强作用。方法:将重组pIRES2-EGFP/IL-37质粒(IL-37组)和pIRES2-EGFP质粒(NC组)分别转染到HeLa细胞。Q-PCR和Western blotting法检测IL-37基因和蛋白表达水平;CCK8法检测NC组、IL-37组、顺铂(DDP)组及IL-37+DDP组细胞活性,计算细胞抑制率;RT-PCR法检测信号转导和转录激活因子3(STAT3)及细胞周期蛋白D1(Cyclin D1)mRNA表达水平。结果:与NC组比较,IL-37组IL-37mRNA和蛋白表达水平明显升高(P0.01)。给药后24~72h,5~15mg·L-1 DDP组HeLa细胞活性受到明显抑制(P0.01);与DDP组比较,IL-37+DDP组HeLa细胞抑制率在处理后48h内明显升高(P0.05);与IL-37组比较,IL-37+DDP组HeLa细胞抑制率在处理后96h内均有升高(P0.05)。与NC组比较,IL-37组STAT3和Cyclin D1mRNA表达水平明显下降(P0.01)。结论:IL-37高表达可抑制宫颈癌细胞的增殖,并能增强DDP对宫颈癌细胞的放疗效果,这种效应的发挥可能与IL-37使STAT3和Cyclin D1表达下调有关。
[Abstract]:Aim: to investigate the cytotoxicity and chemosensitivity of IL-37 to cervical cancer HeLa cells by transfection of interleukin 37 (IL-37) gene into cervical cancer HeLa cells. Methods: the recombinant pIRES2-EGFP/IL-37 plasmid (IL-37 group) and pIRES2-EGFP plasmid (NC group) were transfected into HeLa cells respectively. The expression of IL-37 gene and protein were detected by Q-PCR and Western blotting. The cell activity of NC group, IL-37 group, cisplatin (DDP) group and IL-37 DDP group were detected by CCK8, and the expression of signal transduction and transcription activator 3 (STAT3) and cyclin D1 (Cyclin D1) mRNA were detected by RT-PCR method. Results: the expression of IL-37mRNA and protein in IL-37 group was significantly higher than that in NC group (P0.01). The activity of HeLa cells in DDP group was significantly inhibited (P0.01), and the inhibition rate of HeLa cells in IL-37 DDP group was significantly higher than that in DDP group (P0.05). Compared with IL-37 group, the inhibition rate of HeLa cells in IL-37 DDP group was increased within 96 h after treatment (P0.05). Compared with NC group, the expression of STAT3 and Cyclin D1mRNA in IL-37 group decreased significantly (P0.01). Conclusion: the high expression of IL-37 can inhibit the proliferation of cervical cancer cells and enhance the radiotherapeutic effect of DDP on cervical cancer cells. This effect may be related to the down-regulation of STAT3 and Cyclin D1 expression induced by IL-37.
【作者单位】： 广东医科大学基础医学院组织学与胚胎学教研室;
【基金】：国家自然科学基金资助课题(81302244) 广东省科技厅科技发展计划项目资助课题(2016A020215147,2013B021800062) 广东省卫计委医学科研基金项目资助课题(A2016208,B2013293) 广东省东莞市科技局社会发展重点基金项目资助课题(2013108101051) 广东医科大学科研基金资助课题(M2016028) 广东省湛江市科技局科技计划项目资助课题(2013B01092)
【分类号】：R737.33
[Abstract]:Aim: to investigate the cytotoxicity and chemosensitivity of IL-37 to cervical cancer HeLa cells by transfection of interleukin 37 (IL-37) gene into cervical cancer HeLa cells. Methods: the recombinant pIRES2-EGFP/IL-37 plasmid (IL-37 group) and pIRES2-EGFP plasmid (NC group) were transfected into HeLa cells respectively. The expression of IL-37 gene and protein were detected by Q-PCR and Western blotting. The cell activity of NC group, IL-37 group, cisplatin (DDP) group and IL-37 DDP group were detected by CCK8, and the expression of signal transduction and transcription activator 3 (STAT3) and cyclin D1 (Cyclin D1) mRNA were detected by RT-PCR method. Results: the expression of IL-37mRNA and protein in IL-37 group was significantly higher than that in NC group (P0.01). The activity of HeLa cells in DDP group was significantly inhibited (P0.01), and the inhibition rate of HeLa cells in IL-37 DDP group was significantly higher than that in DDP group (P0.05). Compared with IL-37 group, the inhibition rate of HeLa cells in IL-37 DDP group was increased within 96 h after treatment (P0.05). Compared with NC group, the expression of STAT3 and Cyclin D1mRNA in IL-37 group decreased significantly (P0.01). Conclusion: the high expression of IL-37 can inhibit the proliferation of cervical cancer cells and enhance the radiotherapeutic effect of DDP on cervical cancer cells. This effect may be related to the down-regulation of STAT3 and Cyclin D1 expression induced by IL-37.
【作者单位】： 广东医科大学基础医学院组织学与胚胎学教研室;
【基金】：国家自然科学基金资助课题(81302244) 广东省科技厅科技发展计划项目资助课题(2016A020215147,2013B021800062) 广东省卫计委医学科研基金项目资助课题(A2016208,B2013293) 广东省东莞市科技局社会发展重点基金项目资助课题(2013108101051) 广东医科大学科研基金资助课题(M2016028) 广东省湛江市科技局科技计划项目资助课题(2013B01092)
【分类号】：R737.33
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