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Schematic illustration of IR783‐stabilized nanodrugs to enhance anticancer immune response and promote breast cancer immunotherapy. A) The nanodrugs are formulated with IR783, β ‐lap, and CUDC101. IR783 serves as a stabilizer to form nanoparticles with two hydrophobic drug molecules based on small molecule self‐assembly. B) The nanodrugs can enter breast cancer cells through CAV‐1‐mediated endocytosis pathway and achieve synergistic anticancer effects from NQO1‐dependent oxidation therapy and CUDC101‐provoked epigenetic regulation. C) The nanodrugs can further promote DAMPs release and dendritic cell maturation to boost systemic antitumor immunity and inhibit both primary and distant tumor growth.
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Schematic illustration of IR783‐stabilized nanodrugs to enhance anticancer immune response and promote breast cancer immunotherapy. A) The nanodrugs are formulated with IR783, β ‐lap, and CUDC101. IR783 serves as a stabilizer to form nanoparticles with two hydrophobic drug molecules based on small molecule self‐assembly. B) The nanodrugs can enter breast cancer cells through CAV‐1‐mediated endocytosis pathway and achieve synergistic anticancer effects from NQO1‐dependent oxidation therapy and CUDC101‐provoked epigenetic regulation. C) The nanodrugs can further promote DAMPs release and dendritic cell maturation to boost systemic antitumor immunity and inhibit both primary and distant tumor growth.
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Schematic illustration of IR783‐stabilized nanodrugs to enhance anticancer immune response and promote breast cancer immunotherapy. A) The nanodrugs are formulated with IR783, β ‐lap, and CUDC101. IR783 serves as a stabilizer to form nanoparticles with two hydrophobic drug molecules based on small molecule self‐assembly. B) The nanodrugs can enter breast cancer cells through CAV‐1‐mediated endocytosis pathway and achieve synergistic anticancer effects from NQO1‐dependent oxidation therapy and CUDC101‐provoked epigenetic regulation. C) The nanodrugs can further promote DAMPs release and dendritic cell maturation to boost systemic antitumor immunity and inhibit both primary and distant tumor growth.

Journal: Advanced Science

Article Title: IR783‐Stabilized Nanodrugs Enhance Anticancer Immune Response by Synergizing Oxidation Therapy and Epigenetic Modulation

doi: 10.1002/advs.202415684

Figure Lengend Snippet: Schematic illustration of IR783‐stabilized nanodrugs to enhance anticancer immune response and promote breast cancer immunotherapy. A) The nanodrugs are formulated with IR783, β ‐lap, and CUDC101. IR783 serves as a stabilizer to form nanoparticles with two hydrophobic drug molecules based on small molecule self‐assembly. B) The nanodrugs can enter breast cancer cells through CAV‐1‐mediated endocytosis pathway and achieve synergistic anticancer effects from NQO1‐dependent oxidation therapy and CUDC101‐provoked epigenetic regulation. C) The nanodrugs can further promote DAMPs release and dendritic cell maturation to boost systemic antitumor immunity and inhibit both primary and distant tumor growth.

Article Snippet: β ‐lapachone ( β ‐lap), crystal violet, and DNase I were obtained from Macklin (Shanghai, China).

Techniques:

Preparation and characterization of IR/Lap/CUDC NPs. A) Size distribution and transmission electron microscopy (TEM) image of IR/Lap/CUDC NPs (Scale bar: 200 nm). B) Zeta potential of IR/Lap/CUDC NPs. C) UV–vis absorption spectra of free β ‐lap, CUDC101, IR783, and IR/Lap/CUDC NPs. D) Stability test of IR/Lap/CUDC NPs under physiological conditions for 48 h. E) Size distribution changes of IR/Lap/CUDC NPs after H 2 O 2 incubation. F) Fluorescent spectra of IR/Lap/CUDC NPs with or without H 2 O 2 incubation. G) UV–vis absorption spectra of IR/Lap/CUDC NPs with or without H 2 O 2 incubation. H) Cell viability of 4T1 cells treated with gradient concentrations of free β ‐lap and CUDC101. I) Synergy score of free β ‐lap and CUDC101 in 4T1 cells at gradient concentrations calculated by the Highest Single Agent (HSA) model in SynergyFinder.

Journal: Advanced Science

Article Title: IR783‐Stabilized Nanodrugs Enhance Anticancer Immune Response by Synergizing Oxidation Therapy and Epigenetic Modulation

doi: 10.1002/advs.202415684

Figure Lengend Snippet: Preparation and characterization of IR/Lap/CUDC NPs. A) Size distribution and transmission electron microscopy (TEM) image of IR/Lap/CUDC NPs (Scale bar: 200 nm). B) Zeta potential of IR/Lap/CUDC NPs. C) UV–vis absorption spectra of free β ‐lap, CUDC101, IR783, and IR/Lap/CUDC NPs. D) Stability test of IR/Lap/CUDC NPs under physiological conditions for 48 h. E) Size distribution changes of IR/Lap/CUDC NPs after H 2 O 2 incubation. F) Fluorescent spectra of IR/Lap/CUDC NPs with or without H 2 O 2 incubation. G) UV–vis absorption spectra of IR/Lap/CUDC NPs with or without H 2 O 2 incubation. H) Cell viability of 4T1 cells treated with gradient concentrations of free β ‐lap and CUDC101. I) Synergy score of free β ‐lap and CUDC101 in 4T1 cells at gradient concentrations calculated by the Highest Single Agent (HSA) model in SynergyFinder. "NPs" shown in (E), (F), and (G) refers to IR/Lap/CUDC NPs.

Article Snippet: β ‐lapachone ( β ‐lap), crystal violet, and DNase I were obtained from Macklin (Shanghai, China).

Techniques: Transmission Assay, Electron Microscopy, Zeta Potential Analyzer, Incubation