International journal of nanomedicine · 2026
Metal-Organic Framework Nanoplatform Synergizes Fenton-Driven Ferroptosis and Photodynamic Apoptosis for Enhanced Hepatocellular Carcinoma Therapy.
СтатьяНазвание и аннотация: Перевод в очереди
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Kong Shasha, Lin Hongmei, Liu Yuling, Tang Ruying, Li Hui, Lin Longfei
Аннотация
BACKGROUND: Hepatocellular carcinoma (HCC) is notorious for its dismal prognosis and resistance to conventional therapies. The integration of multiple cell death mechanisms emerges as a promising strategy to combat the heterogeneity of this malignancy.
PURPOSE: Herein, we engineered a multifunctional nanoplatform, TPMIL101-TCPP@Lip-HA, by encapsulating the photosensitizer TCPP and chemotherapeutic agent triptolide (TP) within a metal-organic framework (MIL101), followed by surface modification with liposomes and hyaluronic acid. This sophisticated drug delivery system capitalizes on the enhanced permeability and retention effect to achieve tumor-specific accumulation.
METHODS: Upon reaching the tumor site, TPMIL101-TCPP@Lip-HA undergoes gradual disintegration, releasing its therapeutic payload. The tumor microenvironment facilitates the reduction of Fe³⁺ to Fe²⁺, triggering ferroptosis through the Fenton reaction. Simultaneously, laser irradiation activates TCPP to generate cytotoxic reactive oxygen species, initiating photodynamic therapy-induced apoptosis. The concomitant accumulation of lipid peroxides synergistically amplifies the ferroptotic cascade.
RESULTS: In vitro/in vivo studies confirm potent anti-HCC efficacy with reduced TP toxicity. Mechanistic studies elucidate that TPMIL101-TCPP@Lip-HA orchestrates ferroptosis through modulation of iron storage and lipid oxidation proteins, while concurrently inducing apoptosis via the cytochrome c/Apaf-1/caspase signaling axis.
CONCLUSION: These findings collectively underscore TPMIL101-TCPP@Lip-HA as a potent therapeutic nanoplatform capable of arresting HCC progression.
PURPOSE: Herein, we engineered a multifunctional nanoplatform, TPMIL101-TCPP@Lip-HA, by encapsulating the photosensitizer TCPP and chemotherapeutic agent triptolide (TP) within a metal-organic framework (MIL101), followed by surface modification with liposomes and hyaluronic acid. This sophisticated drug delivery system capitalizes on the enhanced permeability and retention effect to achieve tumor-specific accumulation.
METHODS: Upon reaching the tumor site, TPMIL101-TCPP@Lip-HA undergoes gradual disintegration, releasing its therapeutic payload. The tumor microenvironment facilitates the reduction of Fe³⁺ to Fe²⁺, triggering ferroptosis through the Fenton reaction. Simultaneously, laser irradiation activates TCPP to generate cytotoxic reactive oxygen species, initiating photodynamic therapy-induced apoptosis. The concomitant accumulation of lipid peroxides synergistically amplifies the ferroptotic cascade.
RESULTS: In vitro/in vivo studies confirm potent anti-HCC efficacy with reduced TP toxicity. Mechanistic studies elucidate that TPMIL101-TCPP@Lip-HA orchestrates ferroptosis through modulation of iron storage and lipid oxidation proteins, while concurrently inducing apoptosis via the cytochrome c/Apaf-1/caspase signaling axis.
CONCLUSION: These findings collectively underscore TPMIL101-TCPP@Lip-HA as a potent therapeutic nanoplatform capable of arresting HCC progression.