Microplastics and nanoplastics as potential ecological oncogenic co-drivers: rewiring host-microbe interactions in cancer.
- 1Escuela Profesional de Medicina, Facultad de Ciencias de la Salud, Universidad Nacional de Moquegua, Moquegua, Peru.
- 2Laboratorio de Genética Humana, Facultad de Ciencias Biológicas, Universidad Nacional Mayor de San Marcos, Lima, Peru.
Abstract
Microplastics and nanoplastics (MPs/NPs) are increasingly recognized as biologically active interfaces that may reshape host-microbe interactions in carcinogenesis. This review proposes a hypothesis-generating mechanistic framework in which MPs/NPs may influence cancer-related processes through the integration of environmental exposure, epithelial barrier disruption, immune dysregulation, and tumor microenvironment remodeling. Although applicable to multiple epithelial interfaces, the framework primarily focuses on the intestinal mucosa, where the most substantial evidence exists. Through plastisphere formation, MPs/NPs adsorb pollutants, virulence factors, and microbial communities, potentially facilitating pathogen persistence, horizontal gene transfer, and antibiotic resistance enrichment. Upon host exposure, MPs/NPs have been associated with compromised epithelial integrity, enhanced microbial translocation, and activation of inflammatory pathways involving pattern recognition receptors, NF-κB, and the NLRP3 inflammasome. At the microbiome level, MPs/NPs may promote dysbiosis, alter microbial metabolism, and favor pro-inflammatory and genotoxic metabolites that could reinforce oncogenic signaling. These processes may converge to sustain chronic inflammation, immune evasion, extracellular matrix remodeling, angiogenesis, and tumor-permissive niches. While experimental and biomarker-based evidence support this axis, direct human data remain limited. Collectively, this review provides a conceptual basis for understanding environmentally associated carcinogenesis through MPs/NPs as ecological mediators bridging the environmental exposures, microbiome, and cancer biology.
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BibTeX
@article{poncecusi2026microplastics,
title = {{Microplastics and nanoplastics as potential ecological oncogenic co-drivers: rewiring host-microbe interactions in cancer.}},
author = {Richard Ponce-Cusi and Claudia Barletta-Carrillo and Nesstor Pilco-Ferreto},
journal = {Frontiers in cellular and infection microbiology},
year = {2026},
month = oct,
doi = {10.3389/fcimb.2026.1923626},
url = {https://europepmc.org/article/MED/42903469},
note = {CC BY},
}
RIS
TY - JOUR
TI - Microplastics and nanoplastics as potential ecological oncogenic co-drivers: rewiring host-microbe interactions in cancer.
AU - Richard Ponce-Cusi
AU - Claudia Barletta-Carrillo
AU - Nesstor Pilco-Ferreto
PY - 2026
DA - 2026/10/06
JO - Frontiers in cellular and infection microbiology
DO - 10.3389/fcimb.2026.1923626
UR - https://europepmc.org/article/MED/42903469
AB - Microplastics and nanoplastics (MPs/NPs) are increasingly recognized as biologically active interfaces that may reshape host-microbe interactions in carcinogenesis. This review proposes a hypothesis-generating mechanistic framework in which MPs/NPs may influence cancer-related processes through the integration of environmental exposure, epithelial barrier disruption, immune dysregulation, and tumor microenvironment remodeling. Although applicable to multiple epithelial interfaces, the framework primarily focuses on the intestinal mucosa, where the most substantial evidence exists. Through plastisphere formation, MPs/NPs adsorb pollutants, virulence factors, and microbial communities, potentially facilitating pathogen persistence, horizontal gene transfer, and antibiotic resistance enrichment. Upon host exposure, MPs/NPs have been associated with compromised epithelial integrity, enhanced microbial translocation, and activation of inflammatory pathways involving pattern recognition receptors, NF-κB, and the NLRP3 inflammasome. At the microbiome level, MPs/NPs may promote dysbiosis, alter microbial metabolism, and favor pro-inflammatory and genotoxic metabolites that could reinforce oncogenic signaling. These processes may converge to sustain chronic inflammation, immune evasion, extracellular matrix remodeling, angiogenesis, and tumor-permissive niches. While experimental and biomarker-based evidence support this axis, direct human data remain limited. Collectively, this review provides a conceptual basis for understanding environmentally associated carcinogenesis through MPs/NPs as ecological mediators bridging the environmental exposures, microbiome, and cancer biology.
SN - 2235-2988
ER -