ArticleJournal of nanobiotechnology2026
A Cu-based metal-organic framework based on desloratadine and siHIF-1α for achievement of genes/drugs/CDT combination therapy in hepatocellular carcinoma.
Article in Journal of nanobiotechnology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundDesloratadine (DL) has been demonstrated to inhibit NMT1 enzymatic activity, thereby promoting oxidative stress and endoplasmic reticulum (ER) stress to induce cancer cell death. However, the lack of tumor targeting limits its therapeutic efficacy. The combination of siRNA technology and nanotechnology provides possibility to overcome this limitation. In this study, a Cu-based metal-organic frameworks (MOF) was developed for co-delivery of DL and siHIF-1α to enhance targeted therapy against hepatocellular carcinoma (HCC).
methodThe nanocomposites DL/siHIF-1α@MOF-199@FA was synthesized by loading DL and siHIF-1α into MOF-199, followed by surface modification with folic acid (FA). The physicochemical properties were characterized using transmission electron microscope (TEM), Zeta potential, Fourier transform infrared spectrometer (FTIR), and X-ray Diffraction (XRD). The cell uptake, cell toxicity, and anti-tumor abilities were investigated in Huh7 cells and a xenograft mouse model. Gene/protein expression, ROS production, and biosafety were assessed by qRT-PCR, Western blot, and blood biochemical analysis.
resultsThe obtained DL/siHIF-1α@MOF-199@FA exhibited a particle size of about 178.9 nm with a negative surface charge. FTIR and XRD indicated the successfully loading of DL and siHIF-1α. The DL/siHIF-1α@MOF-199@FA exhibited pH-responsive drug release with accelerated release under acidic conditions (pH 5.5); effectively protected siHIF-1α from nuclease degradation, and presented glutathione (GSH)-responsive structural collapse, accompanied by enhanced hydroxyl radical (•OH) generation. These results indicated the excellent circulation stability and reduced risk of premature release. FA modification significantly enhanced cellular uptake and cytoplasmic localization in Huh7 cells. The anti-tumor ability of DL/siHIF-1α@MOF-199@FA were confirmed in vitro HCC cell lines and an in vivo mouse model. Mechanistically, the nanocomposite successfully delivered functional siHIF-1α and inhibited NMT1 signaling, thereby activating ER stress and oxidative stress. Meanwhile, the DL/siHIF-1α@MOF-199@FA exhibited excellent biocompatibility, no major organ toxicity, and normal blood biochemical parameters.
conclusionThe fabricated DL/siHIF-1α@MOF-199@FA nanocomposite integrates tumor targeting, combined therapeutic modalities (gene/drug/CDT), and favorable biosafety, representing a promising nanoplatform for HCC treatment.
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