Using a human bronchial epithelial cell-based malignant transformation model to explore the function of hsa-miR-200 family in the progress of PM2.5-induced lung cancer development

  • Environ Pollut. 2023 Feb 15;319:120981. doi: 10.1016/j.envpol.2022.120981.
Wanli Ma  1 Lin Xu  1 Xueying Sun  1 Yuan Qi  1 Shen Chen  2 Daochuan Li  2 Yuan Jin  1 Ningning Chen  1 Xiaoxiao Zhu  1 Jiao Luo  1 Chuanhai Li  1 Kunming Zhao  1 Yuxin Zheng  1 Dianke Yu  3
Affiliations
  • 1. Department of Toxicology, School of Public Health, Qingdao University, Qingdao, China.
  • 2. Department of Toxicology, School of Public Health, Sun Yat-sen University, Guangzhou, China.
  • 3. Department of Toxicology, School of Public Health, Qingdao University, Qingdao, China. Electronic address: [email protected].
Abstract

Numerous studies have revealed that ambient long-term exposure to fine particulate matter (PM2.5) is significantly related to the development of lung Cancer, but the molecular mechanisms of PM2.5 exposure-induced lung Cancer remains unknown. As an important epigenetic regulator, MicroRNAs (miRNAs) play vital roles in responding to environment exposure and various diseases including lung Cancer development. Here we constructed a PM2.5-induced malignant transformed cell model and found that miR-200 family, especially miR-200a-3p, was involved in the process of PM2.5 induced lung Cancer. Further investigation of the function of miR-200 family (miR-200a-3p as a representative revealed that miR-200a-3p promoted cell migration by directly suppressing TNS3 expression. These results suggested that ambient PM2.5 exposure may increase the expression of miR-200 family and then promote the proliferation and migration of lung Cancer cells. Our study provided novel model and insights into the molecular mechanism of ambient PM2.5 exposure-induced lung Cancer.

Keywords
Cell migration; Malignant transformation cell model; Particulate matter; TNS3; miR-200 family.
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