张 玉,曹红荣,王珊珊.白细胞介素35对非小细胞肺癌细胞增殖及凋亡的影响[J].肿瘤学杂志,2021,27(7):556-559.
白细胞介素35对非小细胞肺癌细胞增殖及凋亡的影响
Effect of Interleukin 35 on Proliferation and Apoptosis of Non-small Cell Lung Cancer Cells
投稿时间:2021-04-12  
DOI:10.11735/j.issn.1671-170X.2021.07.B008
中文关键词:  肺肿瘤  白细胞介素  增殖  凋亡
英文关键词:lung neoplasms  interleukin  proliferation  apoptosis
基金项目:安徽医科大学校科研基金资助(2019xkj049)
作者单位
张 玉 安徽医科大学第四附属医院 
曹红荣 安徽医科大学第四附属医院 
王珊珊 安徽医科大学第四附属医院 
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中文摘要:
      摘 要:[目的] 评价沉默白细胞介素35(interleukin 35,IL-35)对非小细胞肺癌细胞增殖及凋亡的影响。[方法] 运用短发卡RNA(short hairpin RNA ,shRNA)干扰技术下调IL-35的表达,将转染shRNA的肺癌细胞分为shNC组和shIL35组,采用CCK-8法、流式细胞术分别检测细胞光密度(optical density,OD)值和凋亡率;实时荧光定量PCR(qPCR)和Western blot 实验分别检测Cyclin D1、Bcl-2 mRNA和蛋白表达水平。[结果] 利用shRNA下调A549、H1975细胞中IL-35的表达后,与shNC组相比,shIL35组OD值降低(t=8.452、8.064,P均<0.05),细胞凋亡率增加(t=5.745、4.334,P均<0.05);Cyclin D1、Bcl-2 mRNA和蛋白水平均表达下调(t=4.866、2.806、4.224、7.683,P均<0.05)。[结论] 非小细胞肺癌细胞中IL-35的表达,可通过下调Cyclin D1、Bcl-2基因表达水平来抑制肺癌细胞增殖、促进其凋亡,为临床肺癌治疗提供新思路。
英文摘要:
      Abstract: [Objective] To investigate the effect of silencing interleukin 35(IL-35) on proliferation and apoptosis of non-small cell lung cancer cells. [Methods] The short hairpin RNA(shRNA) interference technology was used to silence the expression of IL-35, and the lung cancer cell lines transfected with shRNA were divided into shNC group and shIL35 group. Then the optical density(OD) value and apoptosis rate of cells were detected respectively by CCK-8 method and flow cytometry, real-time fluorescent quantitative PCR(qPCR) and Western blot were used to detect the mRNA and protein expression of Cyclin D1 and Bcl-2, respectively. [Results] When silencing the expression of IL-35 with shRNA in A549 and H1975 cells, the OD value of shIL-35 group decreased(t=8.452, 8.064, all P<0.05)and the apoptosis rate increased(t=5.745, 4.334, all P<0.05) compared with the shNC group, and Cyclin D1, Bcl-2 mRNA and protein were down-regulated(t=4.866, 2.806, 4.224, 7.683, all P<0.05). [Conclusion] The expression of IL-35 can inhibit the proliferation and promote the apoptosis of lung cancer cells by down-regulating Cyclin D1 and Bcl-2 proteins, it may provide some new ideas for clinical lung cancer gene therapy.
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