Multiple-level validation identifies PARK2 in the development of lung cancer and chronic obstructive pulmonary disease.

ABSTRACT: An important precursor to lung cancer development is chronic obstructive pulmonary disease (COPD), independent of exposure to tobacco smoke. Both diseases are associated with increased host susceptibility, inflammation, and genomic instability. However, validation of the candidate genes and functional confirmation to test shared genetic contribution and cellular mechanisms to the development of lung cancer in patients with COPD remains underexplored. Here, we show that loss of PARK2 (encoding Parkin) increases the expression of proinflammation factors as well as nuclear NF-κB localization, suggesting a role of PARK2 loss in inflammation. Additional exploration showed that PARK2 deficiency promotes genomic instability and cell transformation. This role of PARK2 in inflammation and chromosom

SUBMITTER: Lee S 

PROVIDER: S-EPMC5190090 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature