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Nanoparticle-based Drug Delivery / Cancer, Hypoxia, and Metabolism / Nanoplatforms for Cancer Theranostics · Journal article
Journal of Nanobiotechnology · August 18, 2026
Early or partial results. Treat as a signal, not a conclusion.
This is a preclinical proof-of-concept study demonstrating that a engineered hydroxyapatite nanoparticle system (Art@TMHCNs) can induce tumor-specific calcium overload and suppress tumor growth in a single xenograft model. The work is hypothesis-generating for a potential strategy to overcome multidrug resistance, but lacks comparator arms, human data, and adequately powered replication to support clinical translation claims.
Preclinical in vivo xenograft efficacy study, single-arm. A549/PTX (paclitaxel-resistant lung adenocarcinoma) xenograft model; cells selected for multidrug resistance phenotype and CD44 expression.. Intervention: Art@TMHCNs—hydroxyapatite core–shell nanospheres (47.0 ± 5.0 nm) surface-functionalized with hyaluronic acid and loaded with artemisinin (SERCA inhibitor), designed to induce tumor-specific Ca²⁺ overload..
TMHCNs achieved monodisperse core–shell nanospheres of 47.0 ± 5.0 nm diameter with CD44-mediated tumor targeting. Art@TMHCNs induced sustained, tumor-selective intracellular Ca²⁺ overload and triggered mitochondrial dysfunction and ATP depletion. In A549/PTX xenograft model, Art@TMHCNs achieved complete tumor growth suppression with pronounced tumor-specific calcification and minimal off-target toxicity.
Translation claim ('clinically translatable') is aspirational; no pharmacokinetics, biodistribution, or toxicology data provided in abstract. In A549/PTX xenograft model, Art@TMHCNs achieved complete tumor growth suppression with pronounced tumor-specific calcification and minimal off-target toxicity.
This in vivo result is not yet translatable to clinical practice. Preclinical efficacy in a single tumor model does not establish safety or efficacy in humans; controlled trials and pharmacokinetic/toxicology studies would be needed before clinical advancement.
Single in vivo xenograft model with no comparator arm, surrogate endpoints (tumor growth, calcification), and no clinical data; represents early-stage proof-of-concept for a novel nanoparticle platform.
As stated by the source record.
Quoted from the source exactly as published.
This in vivo result is not yet translatable to clinical practice. Preclinical efficacy in a single tumor model does not establish safety or efficacy in humans; controlled trials and pharmacokinetic/toxicology studies would be needed before clinical advancement.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Multidrug resistance (MDR) remains a central obstacle in cancer therapy, accounting for over 90% of cancer-related mortality. Although calcium overload has emerged as a promising anticancer strategy, its clinical translation is largely limited by insufficient tumor selectivity. Hydroxyapatite nanoparticles (HAPNs) possess intrinsic biocompatibility and the ability to induce tumor-specific Ca 2+ overload; however, conventional synthesis methods often yield polydisperse and aggregation-prone particles, resulting in high dosage requirements and inconsistent antitumor efficacy. Herein, we reported a tumor-targeting monodisperse hydroxyapatite core–shell nanospheres (TMHCNs) fabricated via microfluidic coaxial chips (MCC)-assisted soft-templating strategy to achieve precise physicochemical control for tumor-specific synergistic Ca 2+ overload therapy. FDA-approved components, sebacic acid, glycerol, and polyethylene glycol, were used to compose uniform nanomicelles as soft templates for homogeneous mineralization, enabling reproducible generation of uniform core–shell nanospheres. Subsequent surface functionalization with hyaluronic acid (HA) yielded monodisperse tumor-targeting nanospheres, TMHCNs (47.0 ± 5.0 nm) with enhanced CD44-mediated cellular uptake. The antimalarial drug and sarcoplasmic/endoplasmic reticulum Ca 2+ -ATPase (SERCA) inhibitor, artemisinin (Art), was then selected and encapsulated into TMHCNs to construct the synergistic Ca 2+ overload nanosystem Art@TMHCNs. TMHCNs alone induced sustained and tumor-selective intracellular Ca 2+ overload. Loading the SERCA inhibitor Art further amplified tumor-specific Ca 2+ overload, triggered mitochondrial dysfunction, depleted ATP, and activated both intrinsic and extrinsic apoptotic pathways, thereby effectively reversing MDR. In an A549/PTX xenograft model, Art@TMHCNs achieved complete tumor growth suppression and pronounced tumor-specific calcification with minimal off-target toxicity. This work establishes a precisely engineered, monodisperse hydroxyapatite core–shell platform that amplifies tumor-specific calcium dysregulation and provides a clinically translatable strategy for safe and effective MDR reversal in cancer therapy.
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