Single-atom Ca nanozyme induces glioma loss of life by Ca2+-overload-enhanced catalytic tumor nanotherapy, ferroptosis and synergistic transforming of the immune microenvironment | Journal of Nanobiotechnology

November 16, 2025

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Synthesis technique and microstructure evaluation

We beforehand demonstrated that piezoelectric polymer membranes based mostly on single metallic atoms are efficient by anchoring remoted calcium (Ca) atoms onto nitrogen-doped carbon and polyvinylidene fluoride (PVDF) composites [12]. Drawing on this prior analysis, we designed and improved the method to synthesize CaCN.

ZIF-8 coated Ca (Ca/ZIF-8) was ready by way of a hydrothermal methodology, adopted by calcination to fabricate CaCN (Supplementary Fig. 1). Zinc nitrate hexahydrate, calcium chloride, and dimethylimidazole have been used as uncooked supplies, and synthesis was carried out utilizing a hydrothermal methodology in methanol, adopted by carbonization. Then, acid etching was carried out to not solely take away residual zinc and calcium to keep away from secondary air pollution but additionally to generate extra mesopores on the unique construction of MOF, selling pollutant adsorption and producing extra floor catalytic response lively websites. Morphology research displayed that the introduction of Ca didn’t have an effect on the construction of ZIF. SEM photographs of ZIF-8 and Ca/ZIF-8 supplies depicted comparable common dodecahedron morphology (Supplementary Fig. 2 A). The powder XRD spectrum (Supplementary Fig. 2B) confirmed that ZIF-8 and Ca/ZIF-8 had comparable crystal phases.

The morphological traits of CaCN have been evaluated utilizing transmission electron microscopy (TEM). As illustrated in Fig. 2A, the HR-TEM picture of CaCN after high-temperature pyrolysis nonetheless confirmed an ordinary dodecahedron construction, indicating that high-temperature therapy didn’t have an effect on the construction of the fabric and validating the high-temperature stability of CaCN supplies. In an effort to make clear the existence type of Ca, aberration-corrected HAADF-STEM characterization of atomic decision was carried out. As displayed in Figs. 2B and C, a lot of Ca atoms have been dispersed within the carbon skeleton, additional supporting the anchoring of a single Ca atom within the carbon framework by N and C atoms. In the meantime, the energy-dispersive X-ray component mapping spectrum (EDS) picture introduced that the weather C, N, and Ca have been evenly distributed in CaCN, as delineated in Fig. 2D. As well as, the existence of Ca and N was confirmed by electron vitality loss spectroscopy (EELS). Two peaks at roughly 350 eV and 400 eV have been distributed on the attribute Ca L edge and N Ok edge, respectively, which supplied sturdy proof that Ca exists as single atoms in CaCN (Supplementary Fig. 2 C).

Chemical state and lively website evaluation

The digital construction and native coordination atmosphere of monatomic calcium have been additional decided by X-ray absorption close to edge construction (XANES) and prolonged X-ray absorption superb construction (EXAFS) to disclose the construction of lively websites. On condition that Ca is extremely lively in air, the Ca Ok-edge XANES spectrum of CaO was used as a calibration reference materials. Determine 3B reveals the Ok-space diagram of Ca Ok-edge EXAFS. It’s emphasizing noting that the EXAFS curve of CaCN markedly differed from that of CaO. The CaCN uncorrected Ca Ok-edge Fourier rework (FT) – EXAFS curve confirmed {that a} important peak is at 1.9 Å, attributed to the Ca-N scattering path (Fig. 3C). As introduced in Fig. 3D, the near-edge absorption spectrum of the CaCN catalyst intently matched the calcium-containing reference (CaO), suggesting that the Ca metallic atom in CaCN was in a cationic state. Ca-O (1.8 Å) and Ca-O-Ca (3.1 Å) peaks weren’t detected in Ca/CN, corroborating the presence of solely a single calcium atom in Ca/CN. In the meantime, the quantitative native coordination parameters of the Ca atom have been additional examined by way of least sq. EXAFS becoming (Fig. 3E), uncovering a coordination variety of 4 for the primary shell and a Ca-N bond size of two.27 Å. Moreover, we beforehand demonstrated that the becoming outcomes of EXAFS revealed that the R-factor worth of the Ca-N₄ construction was 0.0044, which is in good settlement with the characterization outcomes of the pattern, indicating that Ca-N₄ is the lively middle of CaCN [12]. These outcomes signified that the Ca atom coordinated with N atoms to type an lively website. Taken collectively, the aforementioned outcomes supplied sturdy proof for the profitable synthesis of CaCN on the Ca – N₄ website by combining atomic dispersed Ca with 4 N atoms.

To additional examine the catalytic efficiency of CaCN, the response kinetics and environmental responsiveness have been evaluated beneath numerous situations. The catalytic exercise, monitored by the oxidation of TMB (3,3′,5,5′-tetramethylbenzidine) to supply a chromogenic product, demonstrated a transparent dependence on catalyst focus and substrate focus (Fig. 3G), with CaCN exhibiting considerably larger exercise in comparison with management supplies (NC, ZIF-8, and clean) (Fig. 3F). In contrast with pure horseradish peroxidase (HRP), CaCN reveals a decrease Km worth and the next obvious Vmax/Km ratio, which confers a relative benefit at sub-millimolar substrate concentrations (Supplementary Fig. 3 A). Temperature-dependent experiments revealed that the response charge elevated with temperature, as evidenced by a extra pronounced absorbance peak at 652 nm beneath 37 °C in comparison with 20 °C (Supplementary Fig. 3B). Moreover, upon publicity to 1064 nm laser irradiation, the response was notably accelerated, attributed to laser-induced fast temperature elevation, highlighting the potential of CaCN for photothermal-enhanced catalysis. The free vitality profile (Fig. 3H) corroborated these observations, indicating that the Ca-N4 lively middle facilitates spontaneous response pathways with a big discount in vitality boundaries. Collectively, these outcomes verify that the distinctive single-atom Ca-N4 construction performs a pivotal function within the superior catalytic efficiency of CaCN beneath various response situations.

CaCN nanozymes induce glioma cell loss of life

The anti-tumorigenic properties of CaCN have been initially assessed on the mobile stage. To look at the results of various concentrations of CaCN on glioma cells, cell viability was decided utilizing Cell Counting Package-8 (CCK-8) assay on LN229 and GSC23 cells handled with gradient concentrations of CaCN, respectively. Subsequent, cell viability curves beneath every focus of nanozyme therapy have been plotted (Fig. 4A), and the IC50 of CaCN in LN229 and GSC23 cells was decided. In the meantime, we evaluated the cytotoxicity of each ZIF-8 and CaCN, and the outcomes confirmed that CaCN exhibited stronger cytotoxicity, which can be attributed to its larger catalytic exercise (Fig. 3F). Particularly, the IC50 was 20.13 µg/ml in LN229 cells and 30.77 µg/ml in GSC23 cells. For subsequent experiments, we chosen concentrations barely above these values to make sure secure organic results, particularly 30 µg/ml for LN229 cells and 40 µg/ml for GSC23 cells. Due to this fact, for subsequent research on TF-CaCN, we chosen the identical experimental focus. We additionally in contrast the toxicity of TF-CaCN between regular astrocyte cells (NHA) and glioblastoma cells (LN229) utilizing CCK8. The outcomes confirmed that the IC50 worth within the NHA cell line was a lot larger than that within the LN229 cell line (Supplementary Fig. 4B), indicating that the distinctive intracellular microenvironment of tumor cells is extra favorable for catalysis by single-atom nanozymes. As a result of tumor cells generate extra H₂O₂ than regular cells, we sought to analyze whether or not H₂O₂ impacts the catalytic efficiency of CaCN inside cells. WB experiments confirmed that beneath therapy with solely 25 µM H₂O₂ for 3 h, apoptosis markers weren’t altered. Nonetheless, when cells have been co-treated with CaCN and H₂O₂, the apoptosis markers have been even larger than these noticed with CaCN alone (Supplementary Fig. 4 C). This means that H₂O₂ enhances the catalytic impact of CaCN inside cells. The inhibitory impact of CaCN on glioma cells was subsequently examined by way of live-dead fluorescence staining (Fig. 4B). The inhibitory impact of CaCN on the proliferative talents of glioma cells was investigated utilizing colony formation assay (Fig. 4C), demonstrating that totally different concentrations of CaCN exerted important inhibitory results on glioma cells (Fig. 4D). After therapy of glioma cells with CaCN on the IC50 focus, visualization beneath TEM depicted that CaCN was intracellularly engulfed by glioma cells and predominantly localized in lysosomes and cytoplasm, while the realm and perimeter of mitochondria in CaCN-treated cells was lowered. In addition to, mitochondrial cristae nearly disappeared in comparison with the mitochondria within the untreated cells (Fig. 4E). These outcomes collectively recommended that CaCN therapy activated related loss of life mechanisms and disrupted the conventional morphology of mitochondria, finally resulting in glioma cell loss of life.

CaCN triggers intracellular calcium overload-induced apoptosis

As is properly documented, Ca²⁺ performs a important function in apoptosis [13]. The buildup of Ca²⁺ in mitochondria results in a sustained enhance in intracellular Ca²⁺ ranges, resulting in mitochondrial dysfunction and finally to mitochondrial rupture and apoptosis. On the whole, when intracellular ROS ranges are excessively excessive, they work together with proteins and set off oxidative reactions that may alter protein construction and performance [14]. Thus, within the presence of excessive ranges of ROS, calcium channels, and pump proteins might endure irreversible desensitization and harm [15]. The extent of intracellular free Ca²⁺ following therapy with totally different concentrations of CaCN was detected utilizing a Fluo-4 AM fluorescent probe (Fig. 5A), which may bind to Ca²⁺ to supply intense inexperienced fluorescence. As anticipated, the fluorescence depth elevated with growing CaCN concentrations, indicating that CaCN elevated intracellular Ca²⁺ ranges. As well as, the MitoTracker Crimson CMXRos probe was employed to find out the diploma of mitochondrial harm elicited by Ca²⁺ overload. Below physiological situations (excessive mitochondrial membrane potential), MitoTracker Crimson CMXRos accumulates within the mitochondrial matrix and produces purple fluorescence. Following mitochondrial harm (low mitochondrial membrane potential), the fluorescence depth decreases (Fig. 5B) [16]. The outcomes uncovered that the fluorescence depth decreased with growing CaCN concentrations, indicating that CaCN-induced calcium overload strongly disrupted the mitochondrial membrane. The calcium pump PMCA4 ATPase is a calcium ion efflux pump current on the cell membrane and concerned within the excretion of calcium ions from tumor cells, and its exercise may be instantly inhibited by ROS [15]. CaCN, owing to its peroxidase-like properties, catalyzes the era of enormous quantities of reactive oxygen species (ROS) within the tumor microenvironment of gliomas at low pH values. Thus, 2’,7’-dichlorodihydrofluorescein diacetate (DCFH-DA) was used to measure ROS ranges in tumor cells, unveiling that ROS ranges have been considerably elevated within the CaCN group, thereby validating the peroxidase-like properties of CaCN (Fig. 5C). Afterward, Western blot evaluation was carried out to detect the expression of calcium-related proteins in glioma cells as a way to analyze the molecular mechanism of calcium overload. Calpain-1 is a calcium-regulated non-lysosomal thiol protease that may be activated by excessive concentrations of Ca²⁺ [17]. WB outcomes confirmed that PMCA4 expression was down-regulated in glioma cells after CaCN therapy, whereas that of Calpain-1 was up-regulated. These outcomes counsel that CaCN generates a considerable amount of ROS inside the cells, and because of the ROS-mediated inhibition of calcium channels, the intracellular Ca²⁺ ranges constantly rise, finally resulting in calcium overload in glioma cells (Fig. 5D). Thereafter, the membrane-permeable Ca²⁺ chelator BAPTA-AM was used to find out the impact of Ca²⁺ overload on apoptosis. The survival charge of CaCN-treated glioma cells was considerably elevated with gradient concentrations of BAPTA-AM, suggesting that CaCN-induced apoptosis was extremely correlated with calcium overload (Fig. 5E).

CaCN, in distinction to traditional calcium-based nanomaterials, induces a rise in calcium ions whereas producing ROS by its POD-like enzyme properties, thereby inhibiting calcium channels and triggering calcium overload.

CaCN triggers intracellular ferroptosis

To establish genes concerned in glioma cell loss of life after CaCN therapy, RNA sequencing (RNA-seq) was carried out on three teams of regular GSC23 cells and three teams of CaCN-treated GSC23 cells. Volcano plots illustrate variations in gene expression in CaCN-treated glioma cells in comparison with the conventional group (Fig. 6A). Moreover, pathway enrichment evaluation of up-regulated differential genes decided that loss of life of CaCN-treated glioma cells was related to pathways such because the immune pathway, apoptotic pathway, ferroptosis pathway, and sensitivity to hypoxia (Fig. 6B). Subsequently, the attainable mechanisms of cell loss of life have been explored, and single-sample gene enrichment evaluation (ssGSEA) highlighted that CaCN can induce ferroptosis (Fig. 6C). The heatmap illustrates variations in consultant genes within the ferroptosis pathway (Fig. 6D).

Not like different programmed cell loss of life processes reminiscent of apoptosis, necrosis, and autophagy, ferroptosis reveals typical mitochondrial phenotypic modifications, together with mitochondrial shrinkage, membrane wrinkling, elevated membrane density, and decreased mitochondrial cristae [18]. That is according to our observations beneath the transmission electron microscope. Ferroptosis is a novel sort of iron-dependent programmed cell loss of life characterised by lipid peroxidation and glutathione depletion [19]. On this examine, the degrees of GSH and MDA have been decided in CaCN-treated glioma cells, observing that the degrees of GSH/GSSG have been decreased and the degrees of MDA have been elevated, suggesting that CaCN induced the ferroptosis of glioma cells (Fig. 6E). Depletion of GSH inactivates GPX4 and induces lipid peroxidation, which in flip promotes ferroptosis. Due to this fact, the lowered expression of GPX4 is a key biomarker of ferroptosis [20]. Along with GPX4, acyl-coenzyme A synthase long-chain member 4 (ACSL4) is one other indicator of ferroptosis [21]. Consequently, the expression ranges of GPX4 and ACSL4 have been detected utilizing PCR and WB. Diminished GPX4 expression and elevated ACSL4 expression ranges have been noticed within the CaCN-treated group in contrast with the management group, implying that CaCN induced ferroptosis (Fig. 6F, G). Move cytometry outcomes additional demonstrated elevated ROS manufacturing in GBM cells after CaCN therapy (Fig. 6H).

CaCN can rework the tumor immune microenvironment

Based on a earlier examine, inflammatory components activate the Nfkb signaling pathway, stimulating tumor cells to synthesize TNF-α [22]. Pathway enrichment evaluation revealed enrichment of immune-related pathways, together with the TNF pathway (Fig. 5B). Performing ssGSEA on the differential genes recognized by way of sequencing demonstrated enrichment of the TNF-α signaling pathway (Fig. 7A). On the identical time, PCR and WB outcomes indicated that CaCN drives TNF-α manufacturing in glioma cells (Fig. 7B, C), and the power of glioma cells to synthesize TNF-α elevated with growing concentrations of CaCN. This impact could also be ascribed to the discharge of related inflammatory components after lysosomal phagocytosis of CaCN.

TNF-α has been evinced to stimulate the polarization of tumor-associated macrophages (TAMs) from the M0 phenotype to the M1 phenotype [23], thereby reversing tumor immunosuppression. Consequently, an growing variety of researchers are specializing in methods to advertise TAM polarization towards the M1 phenotype [24]. To find out the impact of CaCN on the immune microenvironment, the conditioned medium from GL261 and LN229 cells handled with CaCN was cultured with RAW264.7 and Thp1 cells (PMA-treated polarized to M0 macrophages). PCR and WB outcomes revealed elevated expression ranges of iNOS and IL-6 indicators in macrophages cultured within the conditioned media (Fig. 7D, E), suggesting macrophage polarization from the M0 to the M1 phenotype. To keep away from the potential affect of CaCN itself on macrophages, we instantly handled RAW and THP-1 cells with CaCN. PCR outcomes confirmed that CaCN didn’t trigger a big enhance in IL-6 and iNOS expression in macrophages, indicating that the direct impact of CaCN on stimulating macrophage polarization is proscribed (Supplementary Fig. 6 A). Moreover, the immunofluorescence (IF) assay recommended that because the focus of CaCN elevated, there was a extra pronounced diploma of polarization of macrophages cultured within the conditioned medium on the corresponding focus (Fig. 7F), according to the outcomes of WB evaluation. THP-1 macrophages induced to an M0 state with PMA have been individually co-cultured with CaCN-treated glioma cell traces untreated with nanoscale enzymes for 36 h. Subsequent move cytometry evaluation revealed that macrophages demonstrated important polarization in the direction of an M1 phenotype following CaCN therapy (Fig. 7G). Following this, sequencing information and the cibersort algorithm have been employed to investigate the immune infiltration of CaCN-treated glioma cells, which confirmed that CaCN-treated cells activated numerous immune cells, with elevated ranges of M1 macrophages in comparison with controls (Supplementary Fig. 5), corroborating our earlier findings.

As well as, chemokine-related pathways have been additionally enriched (Fig. 6B). This implies that within the presence of CaCN, glioma cells generate chemokines that doubtlessly improve macrophage chemotaxis and infiltration. Consequently, the Transwell co-culture system was used to evaluate macrophage chemotaxis and infiltration following M1 polarization. To simulate TEM, macrophages have been cultured within the higher chamber, and a conditioned medium from glioma cells handled with totally different concentrations of CaCN was positioned within the decrease chamber. The Transwell co-culture system was employed to evaluate macrophage chemotaxis and infiltration following M1 polarization. Briefly, macrophages have been cultured within the higher chamber, whereas a conditioned medium from glioma cells handled with totally different concentrations of CaCN was positioned within the decrease chamber. After 10 h of incubation, a progressive enhance within the stage of macrophage infiltration was famous with growing concentrations of conditioned medium (Fig. 7H).

These outcomes conjointly counsel that CaCN successfully induced TAM polarization towards the M1 phenotype, enhanced TAM infiltration, and exerted a multifaceted inhibitory killing impact on glioma cells.

TF-CaCN successfully enhanced the permeability of the blood-brain barrier

Though single-atom nanozymes can penetrate the blood-brain barrier to some extent, their penetration effectivity is comparatively low. Due to this fact, we launched transferrin (TF) to boost the concentrating on and penetration effectivity of CaCN throughout the blood-brain barrier, thereby enhancing its potential for scientific software.

First, characterization evaluation confirmed the common hydrodynamic diameter of TF-CaCN (Supplementary Fig. 6B), confirming the profitable modification with TF and indicating that the dimensions distribution was inside the anticipated vary. Within the TEM photographs (Fig. 4E), TF-CaCN displayed lipid-like coating surrounding the dense CaCN core, indicative of PEG encapsulation. These vesicular options have been noticed earlier than full lysosomal digestion, according to partial lipid protection. Then we verified in vitro whether or not the addition of the TF ligand in TF-CaCN would alter the unique catalytic effectivity. CCK8 outcomes confirmed that the IC50 values of TF-CaCN and CaCN have been very comparable (Supplementary Fig. 6 C). Then again, WB outcomes indicated that TF-CaCN, like CaCN, can modulate the exercise of calcium ion channel proteins (Supplementary Fig. 6D). The outcomes point out that the TF ligand doesn’t alter the inherent properties of CaCN.

To judge BBB penetration in vitro, we established a Transwell BBB mannequin utilizing bEnd.3 endothelial cells (Fig. 8A). Briefly, 1 × 10^6 bEnd.3 cells have been seeded onto 2% gelatin–precoated inserts and cultured with medium modifications each 3–4 days till barrier formation, as indicated by transendothelial electrical resistance (TEER). When TEER reached roughly 100 Ω·cm², the BBB was thought of efficiently established (Fig. 8B). GBM cells have been cultured within the decrease chamber, whereas CaCN or TF-CaCN was added to the higher (endothelial) aspect of the insert to imitate luminal publicity.

The EdU assay revealed clear variations in nanoparticle penetration. In contrast with CaCN, TF-CaCN therapy resulted in markedly lowered EdU incorporation in GBM cells within the decrease chamber (Fig. 8C). This means that TF-CaCN crossed the endothelial monolayer extra effectively, delivering larger quantities of lively nanozymes to the glioma cells beneath the barrier. Thus, the in vitro outcomes present direct proof that transferrin modification significantly enhances BBB permeability and subsequent antitumor results.

We additional validated these findings in vivo utilizing an intracranial orthotopic glioblastoma mannequin. After tumor implantation, mice have been handled by tail vein injection with both CaCN or TF-CaCN. Survival evaluation demonstrated that mice receiving TF-CaCN survived considerably longer in contrast with these handled with CaCN (Fig. 8D). As well as, H&E staining of mind sections revealed smaller tumor volumes and lowered tumor cell density within the TF-CaCN group (Fig. 8E–F). These in vivo outcomes verify that transferrin conjugation improves the systemic supply of CaCN throughout the BBB and enhances accumulation at tumor websites.

Taken collectively, each the in vitro BBB mannequin and the in vivo glioma mannequin constantly exhibit that transferrin modification considerably improves the BBB penetration potential of CaCN. This supplies sturdy help for using TF-CaCN as a clinically translatable nanosystem able to reaching efficient and focused supply to glioblastoma tissue.

CaCN enhances the efficacy of temozolomide and inhibits tumor proliferation in vivo

Temozolomide (TMZ) is a generally used chemotherapeutic agent for the therapy of glioma and is taken into account the simplest therapeutic agent for glioma owing to its oral administration, potential to penetrate the blood-brain barrier, stability in acidic environments, and low toxicity profile [25]. Regardless of its mixture with different medicine considerably enhancing the survival outcomes of sufferers after surgical intervention, the efficacy of TMZ stays sub-optimal in scientific follow [26]. Of word, glioma resistance to TMZ is the first explanation for chemotherapy failure [27]. Contemplating that a number of research have highlighted the essential function of ferroptosis in conferring drug resistance [28], we posit that the mixture of CaCN and TMZ might improve the killing of tumor cells.

The EDU outcomes confirmed that the mixture therapy of TMZ and TF-CaCN inhibited GBM cell proliferation extra successfully than both therapy alone (Fig. 9A). Certainly, WB outcomes confirmed that the apoptotic impact was considerably enhanced by the co-administration of TMZ and CaCN (Fig. 9B), suggesting that CaCN might synergistically improve the efficacy of TMZ.

Subsequently, we carried out in vivo drug therapy experiments (Fig. 9C). Beginning on day 7 post-tumor implantation, when intracranial tumor progress was established, mice obtained PBS, TMZ, TF-CaCN, or TMZ + TF-CaCN intravenously each different day at a dose of 1 mg/kg for two weeks. Mice in several teams obtained intravenous injections of TMZ, TF-CaCN, or a mixture of each. Survival evaluation and physique weight measurements indicated that the mixture remedy considerably improved the prognosis of glioblastoma-bearing mice in comparison with monotherapies (Fig. 9D, F). In vivo fluorescence imaging additional demonstrated that the mixed therapy successfully suppressed tumor progress (Fig. 9E, G). These findings strongly help that TF-CaCN enhances the therapeutic efficacy of TMZ. Importantly, IHC outcomes demonstrated that CaCN activated peritumoral CD4 and CD8 indicators, indicating that the immune system was activated and altered the immune microenvironment in vivo (Supplementary Fig. 7). As well as, Hematoxylin Eosin (H&E) staining of main organs (coronary heart, liver, spleen, lungs, and kidneys) harvested from handled mice confirmed no important histopathological harm within the TF-CaCN-treated group (Supplementary Fig. 8). General, these outcomes indicated that CaCN nanozymes possessed passable tumor progress inhibitory exercise in vivo.

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Single-atom Ca nanozyme induces glioma loss of life by Ca2+-overload-enhanced catalytic tumor nanotherapy, ferroptosis and synergistic transforming of the immune microenvironment | Journal of Nanobiotechnology

Synthesis technique and microstructure evaluation

Chemical state and lively website evaluation

CaCN nanozymes induce glioma cell loss of life

CaCN triggers intracellular calcium overload-induced apoptosis

CaCN triggers intracellular ferroptosis

CaCN can rework the tumor immune microenvironment

TF-CaCN successfully enhanced the permeability of the blood-brain barrier

CaCN enhances the efficacy of temozolomide and inhibits tumor proliferation in vivo

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