Interaction of polystyrene nanoplastics and Helicobacter pylori modulates gastric cancer cellular functions and metastasis.

Polystyrene nanoplastics (PS-NPs) accumulate in human digestive tissues. They pose health risks as a new pollutant. Chronic infection is the primary risk factor for gastric cancer (GC). This study tested whether PS-NPs and internalize GC cells and their separate or combined exposure on cell proliferation, apoptosis, autophagy, and metastasis. PS-NPs were co-cultured with . A liver metastasis model was established by exposing the GC cell line HGC-27 to PS-NPs alone or to PS-NPs + , which were then injected into nude mice. Scanning electron microscopy (SEM) demonstrated PS-NPs' adhesion to surface. A 100 μg/mL PS-NPs, for 24 h, inhibited bacterial growth and raised reactive oxygen species (ROS) levels inside bacteria. When HGC-27 cells were co-exposed to PS-NPs + , they internalized both agents. This co-exposure elicited a synergistic cytotoxic response, reduced cell viability and proliferation, increased apoptosis, reduced mitochondrial membrane potential, and enhanced autophagosome formation. Exposure to both agents in vivo differed from that observed in vitro. PS-NPs alone promoted liver and lung metastasis and aggravated hepatic lesions, whereas co-exposure showed mixed, context-dependent effects. These findings indicate that PS-NPs associate with in invading gastric cancer cells, thereby modulating multiple carcinogenesis processes. Integrating and models when assessing the potential long-term health risks of PS-NPs in the gastrointestinal environment is inevitable.