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Sulfamethoxazole (SMX) is a significant environmental concern due to its adverse effects and ecological risks. SMX elimination in aquatic environments via photocatalysis presents a viable solution, given its high oxidation potential. However, such a solution remains controversial, primarily due to a lack of selectivity. Here we introduce a molecularly imprinted TiO2@Fe2O3@g-C3N4 (MFTC) photocatalyst designed for the selective degradation of SMX. To assess MFTC's selectivity, we applied it to degrade synthetic wastewater containing SMX alongside interfering species sulfadiazine (SDZ), ibuprofen (IBU), and bisphenol A (BPA). The results demonstrated a selective degradation efficiency rate of 96.8%, nearly twice that of competing pollutants. The molecularly imprinted sites within the catalyst played a crucial role by selectively capturing SMX and enhancing its adsorption, thereby improving catalytic efficiency. The degradation process involved •OH and •O2− free radicals, with a newly proposed double Z-scheme mechanism and potential pathway for SMX degradation by the MFTC photocatalytic system. This study enriches the application of photocatalysis using molecularly imprinted nanocomposite materials for treating complex pollutant mixtures in water.

Abstract Background Pancreatic cancer (PC) is a highly lethal malignancy that requires effective novel therapies. M2 macrophages are abundant in the PC microenvironment and promote cancer progression. Exosomes are emerging mediators of the crosstalk between cancer cells and the microenvironment. This study was conducted to explore the role of M2 macrophage-derived exosomes in PC. Methods Exosomes derived from M2 macrophages were extracted. miR-193b-3p and TRIM62 were overexpressed or silenced to examine their function in PC. Luminescence assays were used to investigate the interaction between miR-193b-3p and TRIM62. Cell proliferation was examined by EdU staining. Would healing and transwell assays were applied to evaluate cell migration and invasion. Co-immunoprecipitation was used to assess the interaction between TRIM62 and c-Myc. Gene and protein expressions were analyzed by quantitative RT-PCR and immunoblotting, respectively. Results M2 macrophage-derived exosomal miR-193b-3p promoted the proliferation, migration, invasion, and glutamine uptake of SW1990 cells. Mechanism study revealed that TRIM62 is a target of miR-193b-3p. TRIM62 inhibited the proliferation, migration, invasion, and glutamine uptake of SW1990 cells by promoting c-Myc ubiquitination. Our data also suggested that TRIM62 expression negatively correlated with miR-193b-3p and c-Myc expression. High-expression of miR-193b-3p and c-Myc predicts poor prognosis, whereas low-expression of TRIM62 predicts poor prognosis in patients with PC. Conclusion M2 macrophage-derived exosomal miR-193b-3p enhances the proliferation, migration, invasion, and glutamine uptake of PC cells by targeting TRIM62, resulting in the decrease of c-Myc ubiquitination. This study not only reveals the mechanism underlying the crosstalk between M2 macrophages and PC cells but also suggests a promising therapeutic target for PC.