Evaluating the mechanisms and therapeutic potential of ZnO nanoparticles as selective anticancer agents for lung malignancies
9 affiliations
- 1Faculty of Allied Medical Sciences, Hourani Center for Applied Scientific Research, Al-Ahliyya Amman University, Amman, Jordan
- 2Department of Pharmacology and Toxicology, College of Pharmacy, Al Farahidi University, Baghdad, Iraq. [email protected]
- 3Department of Biotechnology and Genetics, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India
- 4Department of Medical Oncology, IMS and SUM Hospital, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, 751003, India
- 5Division of Research and Innovation, Uttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Dehradun, Uttarakhand, India
- 6Centre for Research Impact and Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, Punjab, 140401, India
- 7Department of Dentistry, College of Dentistry, The Islamic University, Najaf, Iraq
- 8Department of Medical Analysis, Medical Laboratory Technique College, The Islamic University of Al Diwaniyah, Al Diwaniyah, Iraq
- 9Scientific-Practical Medical Center for Pediatric Oncology, Hematology and Immunology, Tashkent, Uzbekistan
Abstract
Lung cancer's high mortality necessitates refined, targeted therapeutic interventions. Zinc oxide nanoparticles (ZnO NPs) have emerged as promising anticancer agents owing to their distinctive physicochemical characteristics, particularly their pH-dependent solubility, and their preferential toxicity toward malignant cells. This review critically examines the mechanisms, advantages, and limitations of ZnO NPs as a novel therapeutic strategy for lung cancer. The primary antitumor mechanism involves the generation of reactive oxygen species (ROS), which disrupts the cellular redox balance and induces apoptosis. ZnO NPs are shown to trigger apoptosis by compromising mitochondrial integrity, activating caspase cascades, and altering the expression of Bax and Bcl-2 proteins. Furthermore, they impede cancer cell growth by enforcing a G2/M cell cycle arrest. Selectivity is achieved via the enhanced permeation and retention (EPR) effect and electrostatic affinity, wherein their positive surface charge (at physiological pH) promotes binding to anionic cancer cell membranes. Despite these advantages, significant challenges in biocompatibility, long-term toxicity, and in vivo stability must be addressed to facilitate clinical translation. This review underscores the critical need for further research to unlock the full therapeutic potential of ZnO NPs.
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BibTeX
@article{nsairat2026evaluating,
title = {{Evaluating the mechanisms and therapeutic potential of ZnO nanoparticles as selective anticancer agents for lung malignancies}},
author = {Hamdi Nsairat and Waleed K. Abdulsahib and S. Renuka Jyothi and Priya Priyadarshini Nayak and Ashish Singh Chauhan and Siya Singla and Fadhil Faez Sead and Djamila Polatova},
journal = {Discover Nano},
year = {2026},
month = may,
doi = {10.1186/s11671-026-04618-2},
url = {https://doi.org/10.1186/s11671-026-04618-2},
note = {CC BY-NC-ND},
}
RIS
TY - JOUR
TI - Evaluating the mechanisms and therapeutic potential of ZnO nanoparticles as selective anticancer agents for lung malignancies
AU - Hamdi Nsairat
AU - Waleed K. Abdulsahib
AU - S. Renuka Jyothi
AU - Priya Priyadarshini Nayak
AU - Ashish Singh Chauhan
AU - Siya Singla
AU - Fadhil Faez Sead
AU - Djamila Polatova
PY - 2026
DA - 2026/05/25
JO - Discover Nano
DO - 10.1186/s11671-026-04618-2
UR - https://doi.org/10.1186/s11671-026-04618-2
AB - Lung cancer's high mortality necessitates refined, targeted therapeutic interventions. Zinc oxide nanoparticles (ZnO NPs) have emerged as promising anticancer agents owing to their distinctive physicochemical characteristics, particularly their pH-dependent solubility, and their preferential toxicity toward malignant cells. This review critically examines the mechanisms, advantages, and limitations of ZnO NPs as a novel therapeutic strategy for lung cancer. The primary antitumor mechanism involves the generation of reactive oxygen species (ROS), which disrupts the cellular redox balance and induces apoptosis. ZnO NPs are shown to trigger apoptosis by compromising mitochondrial integrity, activating caspase cascades, and altering the expression of Bax and Bcl-2 proteins. Furthermore, they impede cancer cell growth by enforcing a G2/M cell cycle arrest. Selectivity is achieved via the enhanced permeation and retention (EPR) effect and electrostatic affinity, wherein their positive surface charge (at physiological pH) promotes binding to anionic cancer cell membranes. Despite these advantages, significant challenges in biocompatibility, long-term toxicity, and in vivo stability must be addressed to facilitate clinical translation. This review underscores the critical need for further research to unlock the full therapeutic potential of ZnO NPs.
SN - 2731-9229
ER -