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Peer-reviewedCC BY 4.0Toxicology Reports

Micro- and nanoplastics in gastric cancer: A narrative review

4 affiliations
  1. 1School of Pharmacy, Joy University, Vadakkankulam, Tirunelveli Dist, Tamil Nadu, 627 116, India
  2. 2Department of Pharmacy, Sri Shanmugha College of Pharmacy, Sankari, Salem, Tamil Nadu, 637 304, India
  3. 3Department of Pathology, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea
  4. 4Korean Medicine-Based Drug Repositioning Cancer Research Center, College of Korean Medicine, Kyung Hee University, Seoul, 02447, Republic of Korea

Abstract

Micro- and nanoplastics (MNPs), defined as plastic particles smaller than 5 mm and 1 μm, respectively, are ubiquitous environmental contaminants detected in human tissues and typically ingested through food and drinking water. No threshold for adverse health effects has been established. This narrative review synthesizes current evidence on the molecular mechanisms, interactions with Helicobacter pylori, and experimental findings from 2D and 3D gastric cancer models relevant to MNP-induced gastric carcinogenesis. Particle size, shape, polymer type, surface charge, and weathering status influence toxicity. Proposed mechanisms include oxidative stress, mitochondrial dysfunction, chronic inflammation, genotoxicity, gastric dysbiosis, and ferroptosis, mediated by dysregulation of NF-κB, Wnt/β-catenin, MAPK, PI3K/Akt/mTOR, and cGAS-STING signaling. Nanoplastics (~100 nm) may induce ferroptosis via Fosl1 and p53, whereas larger microplastic fragments may activate YAP signaling and promote proliferation. MNPs may also carry persistent organic pollutants and toxic metals and may act synergistically with H. pylori to potentiate mucosal damage. In conclusion, MNPs can plausibly promote gastric carcinogenesis through mechanisms demonstrated in experimental systems, but a causal role in human gastric cancer has not been established. Standardized analytical methods, environmentally realistic exposure models, and large-scale epidemiological studies are needed.

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BibTeX
@article{russel2026micro,
  title = {{Micro- and nanoplastics in gastric cancer: A narrative review}},
  author = {John Singh Russel and Sulekha Khute and Jinwon Choi and Sohyun Park and Muntajin Rahman and Amama Rani and Bonglee Kim and Paranthaman Subash},
  journal = {Toxicology Reports},
  year = {2026},
  month = oct,
  doi = {10.1016/j.toxrep.2026.102358},
  url = {https://doi.org/10.1016/j.toxrep.2026.102358},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Micro- and nanoplastics in gastric cancer: A narrative review
AU  - John Singh Russel
AU  - Sulekha Khute
AU  - Jinwon Choi
AU  - Sohyun Park
AU  - Muntajin Rahman
AU  - Amama Rani
AU  - Bonglee Kim
AU  - Paranthaman Subash
PY  - 2026
DA  - 2026/10/16
JO  - Toxicology Reports
DO  - 10.1016/j.toxrep.2026.102358
UR  - https://doi.org/10.1016/j.toxrep.2026.102358
AB  - Micro- and nanoplastics (MNPs), defined as plastic particles smaller than 5 mm and 1 μm, respectively, are ubiquitous environmental contaminants detected in human tissues and typically ingested through food and drinking water. No threshold for adverse health effects has been established. This narrative review synthesizes current evidence on the molecular mechanisms, interactions with Helicobacter pylori, and experimental findings from 2D and 3D gastric cancer models relevant to MNP-induced gastric carcinogenesis. Particle size, shape, polymer type, surface charge, and weathering status influence toxicity. Proposed mechanisms include oxidative stress, mitochondrial dysfunction, chronic inflammation, genotoxicity, gastric dysbiosis, and ferroptosis, mediated by dysregulation of NF-κB, Wnt/β-catenin, MAPK, PI3K/Akt/mTOR, and cGAS-STING signaling. Nanoplastics (~100 nm) may induce ferroptosis via Fosl1 and p53, whereas larger microplastic fragments may activate YAP signaling and promote proliferation. MNPs may also carry persistent organic pollutants and toxic metals and may act synergistically with H. pylori to potentiate mucosal damage. In conclusion, MNPs can plausibly promote gastric carcinogenesis through mechanisms demonstrated in experimental systems, but a causal role in human gastric cancer has not been established. Standardized analytical methods, environmentally realistic exposure models, and large-scale epidemiological studies are needed.
SN  - 2214-7500
ER  -