Objective:To conduct a comprehensive comparison of the efficacy, safety, and cost-effectiveness of denosumab versus zoledronic acid in patients with bone metastases from solid tumors and multiple myeloma. Methods:A systematic search of PubMed, Web of Science, Embase, and major Chinese databases was performed for studies published up to 30 September 2025. Eligible evidence included randomized controlled trials, cohort studies, and pharmacoeconomic analyses. Random-effects models were applied for quantitative synthesis. The certainty of evidence for key outcomes was assessed using the GRADE framework. Results:Twenty-one studies were included. Moderate-certainty evidence indicates that denosumab likely delays the time to first skeletal-related event (SRE) (HR = 0.85, 95% CI: 0.79-0.93) and time to first and subsequent SREs (HR = 0.86, 95% CI: 0.76-0.97) relative to zoledronic acid. Subgroup analyses demonstrated that this benefit is pronounced in solid tumors but not observed in multiple myeloma. For survival outcomes, moderate-certainty evidence suggests little to no difference in overall survival (HR = 0.97, P = 0.49) or progression-free survival (HR = 0.99, P = 0.86). Low-certainty evidence suggests that denosumab may reduce the risk of any adverse events (OR = 0.70, P = 0.04) and nephrotoxicity (OR = 0.65, P = 0.02). Pharmacoeconomic evaluations revealed marked geographic heterogeneity: denosumab was generally cost-effective in high-income settings with higher willingness-to-pay thresholds, whereas in resource-limited regions, zoledronic acid remained the more economically favorable option. Conclusion:Denosumab probably confers superior protection against SREs in patients with solid tumors and demonstrates a potentially improved renal safety profile compared with zoledronic acid. However, its cost-effectiveness varies substantially across healthcare systems and is strongly shaped by regional pricing structures and willingness-to-pay thresholds. Clinical adoption should therefore consider tumor biology, safety characteristics, and local economic capacity. Systematic review registration:https://www.crd.york.ac.uk/prospero/, identifier CRD420251020691.

BACKGROUND:Halofantrine (halo) is an antimalarial drug that has recently been proven to have the potential to treat Glioblastoma (GBM). OBJECTIVE:The aim of the study is to explore the inhibitory effect of halos on GBM and its mechanism. METHODS:The expression of ATP6V0D2 in GBM was analyzed using the Cancer Genome Atlas (TCGA), the comprehensive database of gene expression, and clinical patient samples. In vitro, we evaluated the inhibitory effect of halo on U251 cells; qPCR, Western blot, and immunofluorescence were used to detect the changes in ATP6V0D2 and autophagy-related genes and proteins. Transmission electron microscopy was used to detect the formation of autophagosomes. A stable ATP6V0D2 knockdown and overexpression model was constructed in U251 cells to verify the criticality of ATP6V0D2. The in vivo anti-tumor effect and mechanism of halo were evaluated using a U251 cell axillary tumor-bearing mouse model (independent experiment repeat number (n = 5) and tail vein administration injection. RESULTS:The expression level of ATP6V0D2 is relatively low in GBM patients. Halo upregulates ATP6V0D2 and induces cytotoxic autophagy (TA) in U251. Knockdown of ATP6V0D2 can inhibit halo-mediated TA and cytotoxicity, while overexpression can enhance these effects. Halo also demonstrated significant anti-GBM activity in vivo, and its mechanism was consistent with the results of in vitro studies. DISCUSSION:This study has preliminarily demonstrated that the anti-malarial drug halo can promote autophagy in GBM cells by upregulating the ATP6V0D2 gene, thereby exerting an anti-GBM effect. So far, no experimental studies have been conducted on the permeability of the blood-brain barrier within the halo body. Furthermore, the potential cardiac toxicity of halo is a point that deserves particular attention. CONCLUSION:Halo triggers cytotoxic autophagy in U251 cells by upregulating ATP6V0D2, establishing the key tumor suppressor factor status of ATP6V0D2 in GBM.

Ovarian cancer (OC) is a common malignant tumor in women, with poor prognosis and high mortality rates. Early diagnosis, screening, and prognostic prediction of OC have long been focal points and challenges in this field. In recent years, machine learning (ML) has gradually demonstrated its unique advantages in the early diagnosis, screening, and prognostic prediction of tumors, including OC.This study aims to analyze global development trends and research hotspots in the application of ML for OC, thereby providing a reference for future research directions. We searched the Web of Science Core Collection (WoSCC) for all publications related to OC and ML from 2004 to 2024, conducting a quantitative analysis using VOSviewer, R software, and CiteSpace. A total of 777 articles were retrieved.The number of publications related to ML and OC has grown continuously over the past 20 years.China led with 254 articles.The most prominent journals include Gynecologic Oncology, Nature, Clinical Cancer Research, Cancer Research, and Journal of Clinical Oncology.Research hotspots are: (a) ML-driven OC biomarker discovery and personalized treatment; (b) ML in tumor microenvironment analysis and resistance prediction; (c) ML in imaging-based diagnosis and risk stratification; (d) ML in multicenter OC studies. ML in OC is currently in a developmental phase and shows promising potential for the future. This study provides researchers and clinicians with a more systematic understanding of research priorities and forthcoming developments in this area.

A drug delivery system based on silybin-conjugated chitosan (CS-SB) polymeric micelles was developed to improve the oral absorption of doxorubicin (DOX). SB was grafted to CS via succinic acid, and CS-SB was identified by 1H NMR and FT-IR. The DOX-loaded micelles were prepared by self-assembly, and the characteristics of micelles, including a small particle size of 167.8 ± 2.3 nm, a high drug loading capacity of 8.59%, and a low critical micelle concentration of 1.3 × 10-5 g/mL, were demonstrated. The micelles showed oral bioavailability of up to 193% versus DOX·HCl. The cytotoxicity test showed the biosafety of CS-SB and the potential of reductive DOX-induced cardiotoxicity. The inhibition of P-gp efflux and CYP3A4 enzyme in CS-SB micelles was confirmed by cellular uptake and enzyme activity inhibition tests. The endocytosis process of micelles was revealed by an endocytosis inhibition test. The findings exhibited the potential of CS-SB micelles in drug delivery.

Objectives: Crebanine, an alkaloid exhibiting sedative, anti-inflammatory, and anticancer properties, remains unexplored in terms of its anticancer potential against colorectal cancer (CRC). This study aims to bridge this knowledge gap, specifically investigating whether crebanine can suppress CRC and elucidating its underlying molecular mechanism. Methods: We employed the MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl tetrazolium bromide) assay, cell scratch assay, and flow cytometry to observe the effects of crebanine on the growth, migration, and apoptosis of CRC SW480 cells, respectively. High-throughput sequencing was employed to detect differentially expressed genes (DEGs) in SW480 cells treated with crebanine. Enriched pathways of these DEGs were identified through Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. Genes exhibiting the highest correlation in the enriched pathway were further analyzed using clinical data from The Cancer Genome Atlas Program (TCGA) public database, utilizing R software. Results: Crebanine effectively inhibited the proliferation, migration, and invasion of SW480 cells, with concentrations of >= 15 mu g/mL promoting apoptosis. Analysis revealed that the function of DEGs linked to the most enriched pathways was associated with immune infiltration by regulatory T cells (Tregs). When analyzed in conjunction with clinical data, the genes exhibiting the highest correlation in the enrichment pathway were found to be directly associated with clinical prognostic survival. Conclusions: Our study demonstrates that crebanine inhibits colorectal cancer by regulating prognostic target genes related to Tregs. This finding offers a novel approach for pharmacological inhibition and Tregs-targeted therapy in CRC.

Background Halofantrine is a drug used to treat malaria, and recent studies have shown that it has potential to treat glioblastoma. Objective To study the inhibitory effect of Halofantrine on glioblastoma and its mechanism. Methods Based on GEO database and clinical samples, the expression difference of ATP6V0D2 gene in glioblastoma was detected. The inhibitory effect of Halofantrine on U251 cells and the expression of ATP6V0D2 gene and autophagy protein at gene and protein levels were detected in vitro. The importance of ATP6V0D2 gene was verified by constructing stable overexpression and overexpression model of ATP6V0D2 gene in U251 cells. The inhibitory effect and mechanism of Halofantrine on axillary tumor model in nude mice were verified in vivo. Results ATP6V0D2 gene was expressed in low level in glioblastoma patients. Halofantrine up-regulates ATP6V0D2 gene mediated U251 cytotoxic autophagy. After ATP6V0D2 knockdown, Halofantrine-mediated cytotoxic autophagy of U251 was inhibited, while overexpression was reversed. In addition, Halofantrine has a good anti-GBM effect in vivo, and its mechanism of action is consistent with in vitro experiments. Conclusion Halofantrine can mediate toxic autophagy of U251 cells through up-regulation of ATP6V0D2. ATP6V0D2 is a key tumor suppressor gene in glioblastoma.

BACKGROUND:Zinc finger C3H1 domain-containing protein (ZFC3H1) is differentially expressed between primary tumor and the normal in most cancers. Additionally, a recent study has suggested that ZFC3H1 could serve as a novel marker for the prognosis of prostate adenocarcinoma (PRAD). However, the relationship between ZFC3H1 expression and the prognostic values in most tumors remains unclear. Our study is mainly for exploring the prognosis of ZFC3H1 in pan-cancer and for further discovering a potential therapeutics target.METHODS:Based on the clinical big data, we performed a pan-cancer analysis of ZFC3H1, including gene expression, survival prognosis, genetic alteration, protein phosphorylation, immune infiltration and enrichment analysis. In addition, Real-Time PCR and Western Blot were used to further confirm the role of ZFC3H1 in the colorectal cancer.RESULTS:We found that ZFC3H1 expression was connected with the prognosis of multiple malignant tumors. Furthermore, we also observed that ZFC3H1 was highly expressed in colorectal cancer through Real-Time PCR and Western Blot. The primary tumors presented higher phosphorylation level of the S655 site in lung adenocarcinoma, colon adenocarcinoma and uterine corpus endometrial carcinoma. ZFC3H1 expression was positively correlated with the immune infiltration of Cancer-associated fibroblasts (CAFs) in some tumors, such as liver hepatocellular carcinoma. And RNA surveillance pathways may be closely associated with the occurrence of tumors.CONCLUSIONS:Our study first reveals that ZFC3H1 could serve as a novel prognostic biomarker of pan-cancer, especially colorectal cancer.

Intracerebral hemorrhage (ICH) is a severe stroke subtype with high disability and mortality, and no effective treatment is available. Previous research on intracerebral hemorrhage secondary brain injury drugs mainly targeted at cell apoptosis, inflammation and oxidative stress, but did not achieve good effects. In recent years, ferroptosis has become a focus concern in neurological diseases. Ferroptosis is a new type of programmed cell death caused by iron-dependent accumulation of lipid peroxides, in which glutathione peroxidase 4 (GPX4) is a key protein affecting ferroptosis. In this study, we used the STRING protein database to predict the proteins that may be co-expressed with GPX4, and studied the ability of Dauricine(Dau) to up-regulate the expression of GPX4 against ferroptosis and neuroprotection after intracerebral hemorrhage in normal cells in vitro, glutathione peroxidase 4 (GPX4) knockdown cells and collagenase injection in vivo in mouse models of intracerebral hemorrhage. The results showed that glutathione reductase (GSR) was a possible co-expression protein with GPX4. Dau could up-regulate the expression of glutathione peroxidase 4 (GPX4) in intracerebral hemorrhage(ICH) model, normal cells and GPX4 knockdown cells in vitro, and simultaneously up-regulate the expression of GSR in ICH mice. Dau could also reduce the levels of iron and lipid peroxidation, and have a neuroprotective effect on intracerebral hemorrhage(ICH) mice. It was tesified that Dauricine(Dau) could inhibit ferroptosis of nerve cells and alleviate brain injury after intracerebral hemorrhage by upregulating glutathione peroxidase 4 (GPX4) and glutathione reductase (GSR) co-expression. Therefore, Dau may be an effective drug for inhibiting ferroptosis and treating intracerebral hemorrhage.

Background:Accumulating evidences have revealed that the abnormal N6-methyladenosine (m6A) modification is closely associated with the occurrence, development, progression and prognosis of cancer. It is noteworthy that m6A modification is widely existed in circRNAs and found its key biological functions in regulating circRNAs metabolism. However, the role of m6A modified circRNAs in colorectal cancer (CRC) remains unknown. To better understand the role of circRNAs in the pathogenesis of CRC, we focus on the relationship between m6A-modified circRNAs and their parental genes.Methods:Arraystar m6A-circRNA epitranscriptomic microarray was used to identify differentially m6A modified circRNAs between CRC and the control group. In addition, TCGA-COAD and GSE106582 cohort were used to identify differentially expressed mRNAs. In this study, we screened the parental genes for which both circRNAs and mRNAs were down-regulated further to analyze, including gene expression, survival prognosis, enrichment analysis. Additionally, Western Blotting was used to further validate the role of the parental gene in CRC.Results:We found that 1405 significantly downregulated circRNAs in CRC by our microarray data. Moreover, we obtained 113 parental genes for which both circRNAs and mRNAs were down-regulated to analyze the relationship with the prognosis of CRC based on TCGA-COAD cohort. And we identified nine potential prognostic genes, including ABCD3, ABHD6, GAB1, MIER1, MYOCD, PDE8A, RPS6KA5, TPM1 and WDR78. And low expression of these genes was associated with poor survival prognosis of the patients with CRC. In addition, we found that TPM1 is downregulated in CRC by western blotting experiment. And the calcium-signaling pathway may involve the process of the CRC progression.Conclusions:We identified nine potential prognostic genes, after analyzed the relationship between the parental genes of m6A modified circRNAs and the progression of CRC. Above all, our study further validated TPM1 can serve as a potentail signature for CRC patients.

脑出血是神经科常见疾病,患者脑出血后继发脑损伤是当今临床治疗的难点.引起脑出血后患者脑损伤的主要原因是神经炎症反应和氧化应激反应,而神经细胞铁死亡(Ferroptosis,简称铁死亡)与二者有着千丝万缕的关系.铁死亡是一种铁依赖性的非凋亡细胞死亡方式,其特征为细胞内铁诱导的脂质活性氧积累引起氧化应激造成细胞死亡.本文就铁死亡与脑出血后脑损伤的关系以及药物治疗的研究进展进行了综述,旨为患者脑出血后继发脑损伤的预防和治疗提供参考.

Alzheimer's disease (AD) is a degenerative disease of the central nervous system characterized by progressive cognitive and memory-related impairment. However, current therapeutic treatments have not proved sufficiently effective, mainly due to the complicated pathogenesis of the disease. In this study, a nano-formulation of graphene oxide (GO) loaded with dauricine (Dau) was investigated in terms of the combined anti-inflammatory and anti-oxidative stress effects of Dau and the inhibition of misfolding and aggregation of the amyloid-β (Aβ) protein by GO. Both in vivo and in vitro models were induced using Aβ1-42, and the formulation was administered nasally in mice. The results showed that GO loaded with Dau greatly reduced oxidative stress through increasing superoxide dismutase levels and decreasing reactive oxygen species and malondialdehyde levels in vitro; it also alleviated the cognitive memory deficits and brain glial cell activation in mice with Aβ1-42-induced AD. This proved that GO loaded with Dau could protect against Aβ1-42-induced oxidative damage and apoptosis in both in vitro and in vivo AD models; therefore, GO loaded with Dau has the potential to be an effective and agent for the rapid treatment of AD.

Background Family with sequence similarity 65 member A (FAM65A), also known as RIPOR1, is differentially expressed between human tumor and non-tumor tissues in kinds of cancers. In addition, it was reported that the product of FAM65A may be a biomarker for cholangiocarcinoma patients. However, there is still no evidence on the relationship between the FAM65A and different types of tumors. Our study is mainly for exploring the prognostic values of FAM65A in pan-cancer and for further discovering a potential therapeutics target. Methods We analyzed FAM65A expression, prognostic values, genetic alteration, protein phosphorylation, immune infiltration and enrichment analysis across different types of human malignant tumors based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) datasets. Additionally, Real-Time PCR (RT-qPCR) was performed to further confirm the roles of FAM65A in the pathogenesis of colorectal cancer. Results We found that FAM65A expression was associated with the prognosis of multiple human tumors, especially colorectal cancer. Moreover, we also observed that FAM65A was highly expressed in colorectal cancer through RT-qPCR. We observed that decreasing phosphorylation level of the S351 locus in colon adenocarcinoma, uterine corpus endometrial carcinoma and lung adenocarcinoma. And the expression of FAM65A was positively related to cancer-associated fibroblasts (CAFs) infiltration in many tumors, such as colon adenocarcinoma. Therefore, FAM65A may be a potential prognostic biomarker of human tumors.

An unprecedented microwave-based strategy is developed to facilitate solid-phase, instantaneous delamination and decomposition of graphite fluoride (GF) into few-layer, partially fluorinated graphene. The shock reaction occurs (and completes in few seconds) under microwave irradiation upon exposing GF to either "microwave-induced plasma" generated in vacuum or "catalyst effect" caused by intense sparking of graphite at ambient conditions. A detailed analysis of the structural and compositional transformations in these processes indicates that the GF experiences considerable exfoliation and defluorination, during which sp2 -bonded carbon is partially recovered despite significant structural defects being introduced. The exfoliated fluorinated graphene shows excellent electrochemical performance as anode materials in potassium ion batteries and as catalysts for the conversion of O2 to H2 O2 . This simple and scalable method requires minimal energy input and does not involve the use of other chemicals, which is attractive for extensive research in fluorine-containing graphene and its derivatives in laboratories and industrial applications.

As serine/threonine-protein kinases, Thousand and One Kinases(TAOKs) are members of the GCKlike superfamily, one of two well-known branches of the Ste20 kinase family. Within the last two decades, three functionally similar kinases, namely TAOK1-3, were identified. TAOKs are involved in many molecular and cellular events. Scholars widely believe that TAOKs act as kinases upstream of the MAPK cascade and as factors that interact with MST family kinases, the cytoskeleton, and apoptosis-associated proteins. Therefore, TAOKs are thought to function in tumorigenesis. Additionally, TAOKs participate in signal transduction induced by Notch, TCR, and IL-17. Recent studies found that TAOKs play roles in a series of diseases and conditions, such as the central nervous system dysfunction, herpes viral infection, immune system imbalance, urogenital system malformation during development, cardiovascular events, and childhood obesity. Therefore, inhibitory chemicals targeting TAOKs may be of great significance as potential drugs for these diseases.

Primary intracerebral hemorrhage (ICH) is a leading cause of long-term disability and death worldwide. Drug delivery vehicles to treat ICH are less than satisfactory because of their short circulation lives, lack of specific targeting to the hemorrhagic site, and poor control of drug release. To exploit the fact that metal ions such as Fe2+ are more abundant in peri-hematomal tissue than in healthy tissue because of red blood cell lysis, we developed a metal ion-responsive nanocarrier based on a phosphonated calix[4]arene derivative in order to deliver the neuroprotective agent dauricine (DRC) specifically to sites of primary and secondary brain injury. The potential of the dauricine-loaded nanocarriers for ICH therapy was systematically evaluated in vitro and in mouse models of autologous whole blood double infusion. The nanocarriers significantly reduced brain water content, restored blood-brain barrier integrity and attenuated neurological deficits by inhibiting the activation of glial cells, infiltration by neutrophils as well as production of pro-inflammatory factors (IL-1β, IL-6, TNF-α) and matrix-metalloprotease-9. These results suggest that our dauricine-loaded nanocarriers can improve neurological outcomes in an animal model of ICH by reducing inflammatory injury and inhibiting apoptosis and ferroptosis.

Aims: Dauricine has been found that has significant neuroprotective effect on Alzheimer's disease (AD), but the mechanism is unclear, so we further investigated the possible mechanism of dauricine on AD. Main methods: Cell counting kit-8 (CCK8) was applied to measure the cytotoxicity of dauricine on SH-SY5Y cells that overexpress the Swedish mutant form of human beta-amyloid precursor protein (APPsw) and control cells (Neo). We used the Cu2+ to induce oxidative damage on APPsw cells, then tested the effect of dauricine on the damage and relative factors including reactive oxygen species (ROS), mitochondrial membrane potential (MMP) and superoxide dismutase (SOD) activity. The secretion level of amyloid beta 1-42(A beta(1-42)), protein expression of apoptosis-related factors and the components of nuclear factor erythroid 2-related factor 2 (Nrf2) pathway were determined by western blotting. A beta(1-42)-transgenic Caenorhabditis elegans GMC101, a model of AD, was applied to evaluate the neuroprotective effect of dauricine through the behavioral experiment and relative anti-oxidative tests. Key findings: In vitro, dauricine decreased the secretion level of A beta(1-42), significantly reduced the level of Cu2+-induced ROS, and restored MMP and SOD activity in APPsw cells. Meanwhile, dauricine could suppress the activation of caspase-3 and to upregulate the expression of Bcl-2. Dauricine also regulated the proteins levels of Nrf2, and Kelch-like ECH-associated protein 1 (Keap1) that is necessary for the activation of Nrf2 in APPsw cell. As oxidative stress induced by A beta or paraquat (PQ), dauricine showed protective effects in the survival experiment of GMC101 worms. Significance: Those data revealed that dauricine has the pharmacological activity of anti-oxidative and antiapoptosis, and shows the potential therapeutic value for AD.

Lead (Pb) is a widespread environmental heavy metal toxicant and chronic Pb exposure can have irreversible effects on memory and cognitive function, which is closely related to dendritic spines. Studies have shown that SNX6 and Homer1 can regulate the growth of dendritic spines. We aimed to investigate the effect of Pb exposure on the dendritic spines in hippocampus, the expression of SNX6 and Homer1 in rats and PC12 cells. The animals were randomly divided to three groups: control group, low lead group and high lead group. PC12 cells were divided into 3 groups: 0 μM, 1 μM and 100 μM Pb acetate. The results showed that the Pb levels in blood and hippocampus of all exposure groups were significantly higher than that of the control group. The morphology of dendritic spines in hippocampus after Pb treatment was changed and the density of dendritic spines was reduced. The expression of SNX6 and Homer1 was decreased in Pb exposed groups compared with the control group. Furthermore, up-regulation of SNX6 expression could reverse the down-regulation of Pb exposure on Homer1. These results indicate that Pb exposure can reduce the expression of SNX6 and lead to a decrease in Homer1 expression, which affects the changes in dendritic spines causing learning and memory impairment.

Curcumin (CCM) has many potential uses in anticancer chemotherapy, but its low water solubility poses a major problem, preventing its translation into clinical use. TPGS is a water-soluble derivative of vitamin E that acts as a surfactant with the ability to form micellar nanoparticles in water. More importantly, TPGS acts as a potent antioxidant that can neutralize intracellular reactive oxygen species (ROS). In this study, we solubilized CCM with TPGS using thin-film rehydration to prepare aqueous formulations containing CCM at clinically relevant concentrations. We found that the minimal TPGS:CCM ratio for producing nanoparticles was 5:1 (w/w): at or above this ratio, stable nanoparticles formed with an average particle diameter of 12 nm. CCM was released from TPGS/ CCM micelles in simulated colonic and gastric fluids. These TPGS/CCM nanoparticles were shown to decrease intracellular ROS levels and apoptosis and inhibited migration of HT-29 human colon cancer cells more potently than free CCM. Pharmacokinetic analysis showed TPGS/CCM to be more bioavailable than free CCM after oral administration to rats. Our results suggest that TPGS/CCM may increase therapeutic efficacy of CCM against colon cancer and merits further investigation in a clinical setting.

Amyloid plaque is a prominent pathologic hallmark in the brains of patients with Alzheimer's disease (AD), and it has been shown to be associated with endoplasmic reticulum (ER) stress response. However the precise regulation mechanism of amyloid-beta (Aβ) toxicity remains unclear. Here, we found that dauricine could activate X-box binding protein 1 (XBP-1; active form XBP-1S) and eukaryotic translation initiation factor eIF2α and thus delay the progression of AD in the Aβ1-42-transgenic Caenorhabditis elegans CL2120. The ER stress response factor XBP-1 can be activated and shows neuroprotective activity through acceleration of Aβ clearance. Our study reveals that dauricine activates the ire-1/xbp-1 and perk/eIF2α pathways of the unfolded protein response, attenuates translation, and enhances ER-associated degradation, which reduces Aβ expression and attenuates Aβ-associated toxicity. On the contrary, xbp-1 depletion counteracts the effects of dauricine on Aβ-associated toxicity. These results underscore the functional relevance of XBP-1 in Aβ toxicity and degradation, and highlight the potentially pharmacodynamic value of dauricine in preventing the progression of AD.

Triple-negative breast cancer (TNBC) is a heterogeneous and clinically aggressive disease with no approved targeted therapy. Curcumin has shown therapeutic potential against TNBC, but it shows low bioavailability and low efficacy when administered as a free drug. Here we describe a novel vehicle for in vivo delivery of curcumin based on the phosphorylated calixarene POCA4C6. Curcumin-loaded POCA4C6 micelles (CPM) were prepared using the thin-film method and they showed a unilamellar structure with an average particle size of 3.86 nm. The micelles showed high curcumin encapsulation efficiency and loading was based on liquid chromatography-tandem mass spectrometry. Studies with cell cultures suggest that CPM can sustainably release curcumin in a pH-dependent manner. The micelles efficiently inhibited proliferation, invasion, migration and tumor spheroid formation by BT-549 human breast cancer cells. These effects involved increased apoptosis and reduced levels of nuclear-catenin and androgen receptor. After injection into tumor xenografts, CPM persisted in the tumor tissue and efficiently inhibited tumor growth without causing obvious systemic toxicity. CPM also significantly reduced levels of CD44(+)/CD133(+) breast cancer stem cells. Our results highlight the potential of CPM as an effective therapy against TNBC.