PM2.5-induced alterations of cell cycle associated gene expression in lung cancer cells and rat lung tissues

- Our study explored and characterized the expressions of cell cycle-associated genes induced by urban PM2.5 in H292 and rat lung tissues.
- The expressions of p53 and CDK2 play a crucial role in the early phase of exposure.
- Cdc2 and cyclin B expressions are important in mid-term, while the expression of p21 was predominant in long-term exposure.
- The degree of PM2.5-induced damage to trachea and lung tissue was time-dependent.

The aim of the current study was to investigate the expression of cell cycle-associated genes induced by fine particulate matter (PM2.5) in lung cancer cell line and tissues. The pulmonary lymph node metastasis cells (H292) were treated with PM2.5in vitro. Wistar rats were used to perform an in vivo study. Rats were randomly assigned to experiment and control groups and those in the experiment group were exposed to PM2.5 once every 15 d, while those in the control group were exposed to normal saline. The cell cycle-associated genes expression was analyzed by real-time PCR. Trachea and lung tissues of rats were processed for scanning electron microscopic (SEM) examinations. Exposure of H292 cells to PM2.5 dramatically increased the expressions of p53 and cyclin-dependent kinase 2 (CDK2) after 24 h of exposure (p < 0.01) and markedly increased the expressions of the cell division cycle 2 (Cdc2) and cyclin B after 48 h of exposure (p < 0.01), while those genes expressions were significantly reduced after 72 h of exposure, at which time the expression of p21 was predominant (p < 0.01). In vivo studies further demonstrated these results. The results of SEM suggested that both of the trachea and lung tissues were damaged and the degree of damage was time-dependent. In conclusion, PM2.5 can induce significantly alterations of p53 and CDK2 in the early phase, Cdc2 and cyclin B in mid-term and p21 in long-term exposure. The degree of PM2.5-induced damage to the trachea and lung tissue was time-dependent.