Possible Links Between PM_2.5-Induced NLRP3 Inflammasome Activation and Its Role in Lung Cancer Progression and Drug Resistance.

Authors

Thanaphat Worawichitchaikun, Pitchapa Wantanachaisaeng, Teerapat Teeppaibul, Prasit Suwannalert

Published in

International journal of molecular sciences. Volume 27. Issue 19. Oct 08, 2026. Epub Oct 08, 2026.

Abstract

The rising incidence of lung cancer is increasingly linked to fine particulate matter (PM_2.5) exposure, highlighting its role as a risk factor of lung carcinogenesis. However, the molecular mechanisms behind PM_2.5 and the disease remain incompletely understood. Exposure to PM_2.5 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 PM_2.5-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 PM_2.5-associated lung cancer drug resistance.

PMID:
42884173
Bibliographic data and abstract were imported from PubMed on 16 Oct 2026.

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