Possible Links Between PM2.5-Induced NLRP3 Inflammasome Activation and Its Role in Lung Cancer Progression and Drug Resistance
- 1Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand
- 2Pathobiology Information and Learning Center, Department of Pathobiology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand
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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BibTeX
@article{worawichitchaikun2026possible,
title = {{Possible Links Between PM2.5-Induced NLRP3 Inflammasome Activation and Its Role in Lung Cancer Progression and Drug Resistance}},
author = {Thanaphat Worawichitchaikun and Pitchapa Wantanachaisaeng and Teerapat Teeppaibul and Prasit Suwannalert},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = oct,
doi = {10.3390/ijms27198931},
url = {https://www.mdpi.com/1422-0067/27/19/8931},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Possible Links Between PM2.5-Induced NLRP3 Inflammasome Activation and Its Role in Lung Cancer Progression and Drug Resistance
AU - Thanaphat Worawichitchaikun
AU - Pitchapa Wantanachaisaeng
AU - Teerapat Teeppaibul
AU - Prasit Suwannalert
PY - 2026
DA - 2026/10/08
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27198931
UR - https://www.mdpi.com/1422-0067/27/19/8931
AB - 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.
SN - 1422-0067
ER -