华南预防医学 ›› 2022, Vol. 48 ›› Issue (4): 443-446.doi: 10.12183/j.scjpm.2022.0443

• 论著 • 上一篇    下一篇

PM2.5通过p38MAPK信号通路对HBE细胞癌基因表达的影响

刘宁1, 郑凯1,2, 蔡颖1,2, 余淑苑1, 季佳佳1, 姜帅1, 蓝涛1, 吴丹茵1, 徐新云1   

  1. 1.深圳市疾病预防控制中心,广东 深圳 518055;
    2.南华大学公共卫生学院
  • 收稿日期:2021-05-06 出版日期:2022-04-20 发布日期:2022-05-31
  • 通讯作者: 徐新云,E-mail:xyxu2008@163.com
  • 作者简介:刘宁(1968—),男,硕士研究生,副教授,研究方向为环境与健康;郑凯(1994—),男,硕士研究生,医师,研究方向为环境分子毒理学;刘宁和郑凯为共同第一作者
  • 基金资助:
    深圳市科技研发项目(JCYJ20190807102205480); 深圳市医学重点学科建设经费(SZXK067)

Effects of PM2.5 on oncogene expression via p38MAPK signal pathway in HBE cells

LIU Ning1, ZHENG Kai1,2, CAI Ying1,2, YU Shu-yuan1, JI Jia-jia1, JIANG Shuai1, LAN Tao1, WU Dan-yin1, XU Xin-yun1   

  1. 1. Shenzhen Center for Disease Control and Prevention, Shenzhen 518055, China;
    2. School of Public Health,University of South China
  • Received:2021-05-06 Online:2022-04-20 Published:2022-05-31

摘要: 目的 探讨大气细颗粒物PM2.5通过p38MAPK信号通路对人支气管上皮(human bronchial epithelial,HBE)细胞癌基因表达的影响。方法 设立空白对照组、PM2.5组、SB203580组、PM2.5+SB203580组。以10 µmol/L的p38MAPK抑制剂SB203580预先处理HBE细胞30 min,接着用无血清DMEM培养基培养24 h作为SB203580组;用50 µg/mL PM2.5染毒24 h作为PM2.5组;用10 µmol/L的SB203580预先处理HBE细胞30 min,然后用50 µg/mL的PM2.5染毒24 h作为PM2.5+SB203580组;应用荧光定量PCR和Western blot检测C-MYCC-FOSK-RASP53p38MAPK基因的mRNA和蛋白质表达水平变化。结果 与对照组比较,PM2.5C-MYCC-FOSK-RASp38MAPK基因表达分别升高54.0%、49.2%、96.1%、74.1%,P53基因表达下降49.1%(均P<0.01)。与PM2.5组比较,PM2.5+SB203580组C-MYCC-FOSK-RASp38MAPK基因表达分别下降21.4%、20.8%、39.3%和21.4%,P53基因表达升高43.1%(P<0.01或P<0.05)。Western blot结果显示,与对照组相比,PM2.5C-MYCC-FOSK-RASp38MAPK蛋白表达分别升高110.6%、46.7%、35.5%、82.8%,P53蛋白表达下降42.7%(均P<0.01)。与PM2.5组比较,PM2.5+SB203580组C-MYCC-FOSK-RAS和p38MAPK蛋白表达分别下降37.7%、16.2%、19.6%和25.9%,P53蛋白表达上升43.5%(P<0.01或P<0.05)。结论 p38MAPK抑制剂明显影响PM2.5对癌基因表达的作用,提示p38MAPK信号通路在PM2.5致癌基因表达作用中发挥重要作用。

关键词: PM2.5, MAPK, p38MAPK, 信号通路, 人支气管上皮细胞, 癌基因

Abstract: Objective To investigate the effects of PM2.5 on oncogene expression via p38MAPK signaling pathway in human bronchial epithelial (HBE) cells. Methods Control group, PM2.5 group, SB203580 group and PM2.5+ SB203580 group were established. HBE cells were treated with 10 µmol/L p38MAPK inhibitor SB203580 for 30 min, then cultured in serum-free DMEM medium for 24 h as SB203580 group; HBE cells were treated with 50 μg/mL PM2.5 for 24 h as PM2.5 group; HBE cells were treated with10 µmol/L SB203580 for 30 min, then exposed to 50 μg/mL of PM2.5 for 24 h as the PM2.5+SB203580 group. The mRNA and protein expression levels of C-MYC, C-FOS, K-RAS, P53 and p38MAPK were detected by real-time PCR and Western blot. Results PCR results showed that compared with the control group, the mRNA expression of C-MYC, C-FOS, K-RAS, p38MAPK in the PM2.5 group increased by 54.0%, 49.2%, 96.1%, 74.1%, and P53 decreased by 49.1%. Compared with the PM2.5 group, the mRNA expression of C-MYC, C-FOS, K-RAS and p38MAPK in the PM2.5+SB203580 group decreased by 21.4%, 20.8%, 39.3%, 21.4%, and P53 increased by 43.1% (P<0.01 or P<0.05). Western blot results showed that compared with the control group, the protein expression levels of C-MYC, C-FOS, K-RAS, p38MAPK in the PM2.5 group increased by 110.6%, 46.7%, 35.5%, 82.8%, and P53 decreased by 42.7% (all P<0.01). Compared with the PM2.5 group, the protein expression levels of C-MYC, C-FOS, K-RAS, p38MAPK in the PM2.5+SB203580 group decreased by 37.7%, 16.2%, 19.6%, 25.9%, and P53 increased by 43.5% (P<0.01 or P<0.05). Conclusion The p38MAPK inhibitor obviously influenced the effects of PM2.5 on oncogene expression, indicating that p38MAPK signaling pathway plays an important role in PM2.5-induced oncogene expression.

Key words: PM2.5, Mitogen-activated protein kinase, p38MAPK, Signal pathway, Human bronchial epithelial cells, Oncogene

中图分类号: 

  • R122