Atmospheric particulate matter with aerodynamic diameter ≤10 μm (PM10) is a risk factor for the development of lung cancer, but cellular pathways are not completely understood. STAT3 is a p21Waf1/Cip1 transcription factor and is associated with proliferation and cell survival and is upregulated in lung cancer. PM10 exposure induces p21Waf1/Cip1 expression, which could be related to STAT3 activation. The aims of this work were to investigate whether STAT3 was activated on lung epithelial cells after PM10 exposure and to determine whether or not STAT3 could have an impact on cell cycle distribution and cell survival. Our results showed that PM10 induced STAT3 activation through Src and PKCζ kinases, and it is partially responsible for the p21Waf1/Cip1 induction that was also observed. Moreover, PM10 induced G1-G0 cell cycle arrest. The inhibition of STAT3 phosphorylation prevented cell cycle arrest and triggered apoptosis. These results suggest that PM10 exposure might activate a survival pathway related to STAT3 activation, similar to what has been described as part of the immune system and apoptosis evasion during tumor promotion and development.
- Atmospheric particulate matter (PM)
- PKCζ kinase
- Src kinase
ASJC Scopus subject areas
- Health, Toxicology and Mutagenesis