Find in Library

Telomeres, potential biomarkers of aging, are known to shorten with continued cigarette smoke exposure. In order to further investigate this process and its impact on cellular stress and inflammation, we used an in vitro model with cigarette smoke extract (CSE) and observed the downregulation of telomere stabilizing <i>TRF2</i> and <i>POT1</i> genes after CSE treatment. <i>hTERT</i> is a subunit of telomerase and a well-known oncogenic marker, which is overexpressed in over 85% of cancers and may contribute to lung cancer development in smokers. We also observed an increase in <i>hTERT</i> and <i>ISG15</i> expression levels after CSE treatment, as well as increased protein levels revealed by immunohistochemical staining in smokers’ lung tissue samples compared to non-smokers. The effects of <i>ISG15</i> overexpression were further studied by quantifying <i>IFN-γ</i>, an inflammatory protein induced by <i>ISG15</i>, which showed greater upregulation in smokers compared to non-smokers. Similar changes in gene expression patterns for <i>TRF2</i>, <i>POT1</i>, <i>hTERT</i>, and <i>ISG15</i> were observed in blood and buccal swab samples from smokers compared to non-smokers. The results from this study provide insight into the mechanisms behind smoking causing telomere shortening and how this may contribute to the induction of inflammation and/or tumorigenesis, which may lead to comorbidities in smokers.