Possible Links Between PM2.5-Induced NLRP3 Inflammasome Activation and Its Role in Lung Cancer Progression and Drug Resistance

Information from the abstract

The rising incidence of lung cancer is increasingly linked to fine particulate matter (PM2.5) exposure, highlighting its role as a risk factor of lung carcinogenesis. However, the molecular mechanisms behind PM2.5 and the disease remain incompletely understood. Exposure to PM2.5 triggers inflammatory processes, primarily via ROS overproduction, which activates the NLRP3 inflammasome, a cytosolic NOD-like pattern recognition receptor protein complex that cleaves caspase-1 and drives maturation of pro-interleukin-1β (IL-1β) and pro-interleukin-18 (IL-18), leading to chronic pulmonary inflammation. Based on current evidence, this review displays PM2.5-induced ROS upregulation as an essential trigger of NLRP3 inflammasome activation in lung cancer development and progression and hypothesises that the signalling of NLRP3 may contribute to molecular pathways associated with lung cancer drug resistance. There have been uses of NLRP3 inhibitors in clinical trials of different inflammatory diseases, but none has yet reached clinical testing in oncology. We propose the potential of NLRP3 as a possible prognostic marker and a therapeutic target for PM2.5-associated lung cancer drug resistance.

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Related topics: Inflammasome and immune disorders · Air Quality and Health Impacts · Neutrophil, Myeloperoxidase and Oxidative Mechanisms