Defect engineering synergistically boosts the catalytic activity of Fe-MoO for highly efficient breast mesh antitumor therapy.

The demand for breast mesh with antitumor properties is critical in post-mastectomy breast reconstruction to prevent local tumor recurrence. Molybdenum-based oxide (MoO) exhibits enzyme-like activities by catalyzing endogenous hydrogen peroxide to produce reactive oxygen species for inducing tumor cell apoptosis. However, its catalytic activity is limited by insufficient active sites. Herein, a defect engineering strategy is proposed to create redox nanozymes with multiple enzymatic activities by incorporating Fe into MoO (Fe-MoO). Fe-MoO is subsequently integrated into polycaprolactone (PCL) to fabricate breast meshes for establishing an enzyme-catalyzed antitumor platform. The doping of Fe into MoO formed numerous defect sites, including oxygen vacancies (OV) and Fe substitution sites, synergistically boosting the binding capacity and catalytic activity of Fe-MoO. Density functional theory calculations demonstrated that the outstanding peroxidase-like catalytic activity of Fe-MoO resulted from the synergy between OV and Fe sites. Additionally, OV contributes to the localized surface plasmon resonance effect, enhancing the photothermal capability of the PCL/Fe-MoO mesh. Upon near-infrared laser exposure, the catalytic activity of the PCL/Fe-MoO mesh is further improved, leading to increased generation of reactive oxygen species and enhanced antitumor efficacy, achieving 86.7% tumor cell mortality, a 264% enhancement compared to the PCL/MoO mesh.