Recent studies have identified correlations between cigarette smoke-induced microRNA (miRNA) expression and different aspects of lung cancer; however, it is unclear how miRNA expression directly contributes to carcinogenesis. MiRNAs regulate the expression of target genes and can have a significant impact on when and how well different gene products are expressed. In this issue of the Journal of Clinical Investigation, David Schrump and colleagues at the National Cancer Institute in Bethesda, MD, measured miRNA expression in normal human lung cells exposed to cigarette smoke condensate (CSC) and lung cancer cells derived from smokers and non-smokers. They found that CSC exposure repressed the miRNA miR-487b. Loss of miR-487b increased the expression of several oncogenes and enhanced the proliferation, invasion, tumorigenicity, and metastatic capacity lung cells. Loss of miR-487b and concomitant up-regulation of the five oncogenes was also observed in patient lung cancer specimens. These results reveal a direct mechanism by which cigarette smoke-induced miRNA alterations promote lung carcinogenesis.
|Contact: Jillian Hurst|
Journal of Clinical Investigation