Affiliations 

  • 1 School of Pharmacy, Faculty of Medical Sciences, The University of the West Indies, St. Augustine, Trinidad & Tobago, West Indies
  • 2 USF Health Taneja College of Pharmacy, University of South Florida, Tampa, FL 33612, USA
  • 3 Graphic Era (Deemed to be University) Clement Town Dehradun, 248002, India; Graphic Era Hill University Clement Town Dehradun, 248002, India. Electronic address: pantpharma889@outlook.com
  • 4 Centre for Global Health Research, Saveetha Medical College, Saveetha Institute of Medical and Technical Sciences, Saveetha University, India; Department of Pharmacology, Kyrgyz State Medical College, Bishkek, Kyrgyzstan
  • 5 College of Technical Engineering, The Islamic University, Najaf, Iraq; College of Technical Engineering, The Islamic University of Al Diwaniyah, Al Diwaniyah, Iraq
  • 6 Chandigarh Pharmacy College, Chandigarh Group of Colleges, Jhanjeri, Mohali, Punjab 140307, India
  • 7 Department of Medicine, National Institute of Medical Sciences, NIMS University Rajasthan, Jaipur, India
  • 8 School of Applied and Life Sciences, Division of Research and Innovation, Uttaranchal University, Dehradun, India
  • 9 Centre for Research Impact & Outcome-Chitkara College of Pharmacy, Chitkara University, Punjab
  • 10 Department of Pharmacology, College of Pharmacy, King Khalid University, Abha, Asir 61421, Saudi Arabia
  • 11 Department of Biochemistry, Faculty of Medicine, Bioscience, and Nursing, MAHSA University, Jenjarom, Selangor 42610, Malaysia
Pathol Res Pract, 2024 Jul 01;260:155444.
PMID: 38986361 DOI: 10.1016/j.prp.2024.155444

Abstract

Lung cancer is still a global health challenge in terms of high incidence, morbidity, and mortality. Recent scientific studies have determined that pyroptosis, a highly inflammatory form of programmed cell death, can be identified as a potential lung cancer therapeutic target. The NLRP3 inflammasome acts as a critical mediator in this process and, upon activation, activates multiprotein complex formation as well as caspase-1 activation. This process, triggered by a release of pro-inflammatory cytokines, results in pyroptotic cell death. Also, the relationship between the NLRP3 inflammasome and lung cancer was justified by its influence on tumour growth or metastasis. The molecular pathways produce progenitive mediators and remake the tissue. Finally, targeting NLRP3 inflammasome for pyroptosis induction and inhibition of its activation appears to be a promising lung cancer treatment approach. This technique makes cancer treatment more promising and personalized. This review explores the role of NLRP3 inflammasome activation and its possibilities in lung cancer treatment.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.