Microplastics and nanoplastics as potential ecological oncogenic co-drivers: rewiring host-microbe interactions in cancer.

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.