Chronic Obstructive Pulmonary Disease (COPD) and lung cancer: is the inflammasome at the cross-talk?

COPD and lung cancer (herein, non-small cell lung cancer, NSCLC) are worldwide health concerns. Epidemiological evidence highlight that COPD patients are 6.35 times more likely to develop lung cancer compared to the normal population, supporting the concept that COPD is one of the driving factors of lung cancer establishment. Because these two diseases share common etiological insults, i.e. cigarette smoke (CS) and environmental pollution, and common threatening lung-associated chronic inflammation, the main goal of this review is to describe what so-far identified as molecular/cellular mechanism/s that link COPD to lung cancer. Our data support the role of the inflammasome in both COPD and lung cancer establishment. In particular, we found that absent in melanoma 2 (AIM2) inflammasome paves the way for chronic inflammatory conditions at the basis of both COPD and NSCLC, standing at the crossroad for lung carcinogenesis. We believe that tracking down pathways and molecular interactions related to the inflammasome could open new prospective for therapeutic strategies for both COPD and NSCLC.

Impact statement

Four out of ten COPD patients develop NSCLC, implying that COPD-related inflammatory patterns can pave the way for lung cancer, which represents the first-in-class tumor-derived death. We found that AIM2 inflammasome is highly expressed in smoker subjects who develop COPD leading to NSCLC, opening new perspective for a potential therapeutic target.