A Dual-Stimuli Responsive Nanoplatform via Atomic Layer Deposition of Gold on CoFe2O4 for Thermally Gated Doxorubicin Delivery in Colorectal Cancer.
Targeted chemotherapy for colorectal cancer is often limited by nonspecific drug distribution and systemic toxicity. To improve local therapeutic efficacy and reduce side effects, we designed a thermally gated, dual-stimuli-responsive nanoplatform for controlled doxorubicin (DOX) delivery.
CoFe2O4 (CFO) nanocubes were synthesized and coated with Au nanoparticles via atomic layer deposition (ALD) to obtain CFO/Au nanocomposites with enhanced photothermal properties while retaining magnetic responsiveness. The optimal sample (CFO/Au-2) was further modified with poly(acrylic acid) (PAA) to improve aqueous dispersibility and provide abundant carboxyl groups for DOX loading, yielding CFO/Au-2/PAA/DOX. A thermal gate was then constructed using 1-tetradecanol (TD), a phase-change material with a melting point of ~38 °C, to obtain CFO/Au-2/PAA/DOX/TD. The structural, magnetic, and photothermal properties, DOX loading and release behavior, and in vitro cytotoxicity against SW620 colorectal cancer cells were systematically evaluated under near-infrared (NIR) irradiation and/or alternating magnetic field (AMF).
CFO/Au-2/PAA/DOX/TD exhibited a high DOX loading capacity (~26 wt%) and good colloidal stability. Minimal DOX leakage occurred at physiological temperature, confirming effective encapsulation by solid TD. Under NIR and/or AMF stimulation, the nanocomposite generated pronounced local heating, induced TD melting, and triggered rapid DOX release, with the combined NIR + AMF condition producing the fastest release profile. In vitro, the carrier without DOX showed minimal cytotoxicity toward SW620 cells, whereas CFO/Au-2/PAA/DOX/TD under dual stimulation produced significantly enhanced cytotoxicity toward SW620 cells compared with free DOX at the same drug concentration.
This ALD-engineered CFO/Au-2/PAA/DOX/TD nanoplatform integrates magnetic and photothermal heating with thermally gated, dual-stimuli-responsive drug release, enabling precise spatiotemporal control of DOX delivery. The results suggest strong potential for combined and localized colorectal cancer therapy with reduced systemic toxicity.
CoFe2O4 (CFO) nanocubes were synthesized and coated with Au nanoparticles via atomic layer deposition (ALD) to obtain CFO/Au nanocomposites with enhanced photothermal properties while retaining magnetic responsiveness. The optimal sample (CFO/Au-2) was further modified with poly(acrylic acid) (PAA) to improve aqueous dispersibility and provide abundant carboxyl groups for DOX loading, yielding CFO/Au-2/PAA/DOX. A thermal gate was then constructed using 1-tetradecanol (TD), a phase-change material with a melting point of ~38 °C, to obtain CFO/Au-2/PAA/DOX/TD. The structural, magnetic, and photothermal properties, DOX loading and release behavior, and in vitro cytotoxicity against SW620 colorectal cancer cells were systematically evaluated under near-infrared (NIR) irradiation and/or alternating magnetic field (AMF).
CFO/Au-2/PAA/DOX/TD exhibited a high DOX loading capacity (~26 wt%) and good colloidal stability. Minimal DOX leakage occurred at physiological temperature, confirming effective encapsulation by solid TD. Under NIR and/or AMF stimulation, the nanocomposite generated pronounced local heating, induced TD melting, and triggered rapid DOX release, with the combined NIR + AMF condition producing the fastest release profile. In vitro, the carrier without DOX showed minimal cytotoxicity toward SW620 cells, whereas CFO/Au-2/PAA/DOX/TD under dual stimulation produced significantly enhanced cytotoxicity toward SW620 cells compared with free DOX at the same drug concentration.
This ALD-engineered CFO/Au-2/PAA/DOX/TD nanoplatform integrates magnetic and photothermal heating with thermally gated, dual-stimuli-responsive drug release, enabling precise spatiotemporal control of DOX delivery. The results suggest strong potential for combined and localized colorectal cancer therapy with reduced systemic toxicity.