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. 2025 Jul 14;25(30):11515–11519. doi: 10.1021/acs.nanolett.5c02826

A Strategic Antimetastatic Solution for Bone-Targeting Prostate Cancer via Nanoengineered Niclosamide

Sanoj Rejinold N †, Geun-woo Jin ‡, Jin-Ho Choy †,§,*
PMCID: PMC12314900  PMID: 40657731

Abstract

Prostate cancer is the second leading cause of cancer-related deaths in men worldwide, with bone metastasis being the predominant driver of morbidity and mortality in advanced stages. This underscores the urgent need for innovative therapeutic strategies to address skeletal metastasis and improve patient outcomes. Niclosamide, a long-standing anthelminthic drug, has emerged as a promising multipathway modulator against cancer hallmarks. Here, we propose a nanotechnology-enabled repurposing of niclosamide, hypothesizing that its formulation into smart, targeted nanohybrids could not only suppress prostate tumor growth but also inhibit its dissemination to the skeletal system. We discuss the molecular rationale, design considerations, and translational outlook for nanoengineered niclosamide in the context of metastatic prostate cancer.

Keywords: Niclosamide, Extracellular Matrix (ECM), Aggressive Prostate Cancer, Drug Repurposing, Tumor Microenvironment Modulation

Prostate cancer often follows a distressing trajectory, with primary tumors exhibiting a strong tendency to metastasize to bone, resulting in debilitating pain, pathological fractures, and markedly diminished patient survival. Despite advances in hormone therapy and radiopharmaceuticals, effective control of metastatic lesions remains elusive. The tumor microenvironment of bone, rich in osteotropic factors, facilitates this colonization, urging a paradigm shift from cytotoxic to microenvironment-modulating therapies.

Niclosamide has garnered interest as a potent inhibitor of signaling pathways such as Wnt/β-catenin, STAT3, NF-κB, and Notcheach pivotal in prostate cancer metastasis and bone tropism. − However, its clinical translation is hindered by poor solubility and bioavailability. Nanotechnology offers a transformative strategy to overcome these pharmacokinetic barriers and enable site-specific delivery. −

Molecular Basis of Bone Metastasis in Prostate Cancer

Bone tropism in prostate cancer involves a complex interplay of cancer cell-intrinsic factors and bone niche components (Scheme ). Osteomimicry, , where cancer cells adopt osteoblastic properties, enables their survival and proliferation within the bone matrix.

1. Disruption of Bone Homeostasis and the Vicious Cycle of Bone Metastasis in Advanced Prostate Cancer. (A) Schematic Representation of Prostate Cancer Progression Showing Cancer Cell Leakage from the Primary Tumor Site into Circulation, Facilitating Metastasis to Distant Organs Such as Bone; (B) Left Panel (Bone Homeostasis). Right Panel (Vicious Cycle of Bone Metastasis). Bottom Panel: Therapeutic Agents Like Bisphosphonates (Inhibiting Osteoclast Activity) and Denosumab (Blocking RANKL) Are Used to Manage Skeletal-Related Events by Interrupting This Feedback Loop .

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a Under normal conditions, bone remodeling is tightly regulated by a balance between osteoblast-mediated bone formation and osteoclast-mediated bone resorption.

b Prostate cancer cells localize to the bone microenvironment, where they disrupt this balance. Tumor-secreted factors (e.g., PTHrP, IL-6, TNF-α) stimulate osteoblasts to express RANKL, which activates osteoclasts, leading to excessive bone resorption. In turn, osteoclast activity releases growth factors from the bone matrix that further support tumor growth, perpetuating the cycle.

c Created using Biorender.com.

Niclosamide as a Multitargeted Antimetastatic Agent

The CXCL12/CXCR4 axis and RANK/RANKL signaling promote prostate cancer skeletal metastasis by enhancing tumor cell migration, adhesion, and survival within the bone microenvironment.

Niclosamide suppresses these pathways by inhibiting CXCR4-mediated migration and RANKL-induced NF-κB/MAPK signaling, thereby disrupting the bone-tropic metastatic niche.

Aberrant Wnt/β-catenin and STAT3 activation contribute to therapy resistance and metastatic progression by maintaining cancer stemness and promoting the epithelial–mesenchymal transition.

Niclosamide inhibits both β-catenin and STAT3 signaling, reducing drug-resistant tumor growth and invasive potential in prostate cancer models ,

The androgen receptor splice variant AR-V7 is increasingly recognized as a key driver of bone metastasis in castration-resistant prostate cancer. Previous studies have shown that AR-V7 activates a distinct transcriptional program enriched for metastasis-related genes, including SOX9, and induces osteoblastic bone lesions in vivo. Niclosamide, an FDA-approved drug, has been reported to promote proteasome-mediated degradation of AR-V7 and suppress its transcriptional activity. Therefore, niclosamide is expected to inhibit AR-V7-mediated bone metastasis and may represent a promising therapeutic strategy in advanced prostate cancer.

To further elucidate its comprehensive effects, Table summarizes the molecular targets and mechanistic pathways modulated by niclosamide in advanced prostate cancer and bone metastasis. This includes its impact on Wnt/β-catenin, STAT3, NF-κB, mitochondrial uncoupling, EMT disruption, and tumor-associated macrophages (TAMs), along with the inhibition of osteoclastogenesis and autophagy. These effects contribute to reduced metastasis, enhanced apoptosis, improved drug sensitivity, and preservation of bone integrity. Notably, nanohybrids of niclosamide augment these benefits by enabling sustained, site-specific action within metastatic bone niches.

1. Molecular Targets and Mechanistic Pathways of Niclosamide in Advanced Prostate Cancer and Bone Metastasis. This Table Summarizes the Key Biological Mechanisms Targeted by Niclosamide in the Context of Advanced Prostate Cancer, Particularly Their Role in Mitigating Bone Metastasis. Each Row Outlines a Specific Target or Pathway, Its Contribution to Disease Progression, and the Therapeutic Benefit Conferred by Niclosamide, Including Its Enhanced Impact When Delivered via Nanohybrids.

Mechanism/Target Pathway/Effect Role in Advanced Prostate Cancer Therapeutic Impact of Niclosamide Ref
Wnt/β-catenin inhibition Blocks nuclear β-catenin signaling Involved in tumor progression, EMT, and bone tropism Suppresses metastasis and reduces cancer stemness
STAT3 inhibition Blocks STAT3 phosphorylation and transcriptional activity Promotes proliferation, immune evasion, and M2 macrophage polarization Reverses immune suppression and halts tumor growth
NF-κB inhibition Inhibits pro-inflammatory gene expression Drives chronic inflammation and osteoclast activation in bone metastasis Reduces inflammatory osteolysis and tumor-induced bone destruction
Mitochondrial uncoupling Disrupts oxidative phosphorylation and ATP production Tumor cells rely on mitochondrial metabolism for survival in bone niche Induces energetic crisis and apoptosis in metastatic cancer cells
Disruption of EMT Downregulates mesenchymal markers (e.g., vimentin, N-cadherin) EMT facilitates migration, invasion, and bone colonization Inhibits metastasis initiation and dissemination
CAF modulation Inhibits TGF-β and LOX signaling pathways CAFs remodel ECM and promote metastasis, fibrosis, and resistance Reduces ECM stiffness, blocks pseudoresistance, and improves drug penetration
Macrophage polarization (TAMs) Reprograms M2-like (pro-tumoral) macrophages to M1 (antitumoral) phenotype M2 TAMs support tumor growth, angiogenesis, and bone invasion Enhances antitumor immunity and disrupts metastatic niche
Osteoclastogenesis suppression Inhibits RANKL-mediated osteoclast differentiation Osteoclasts drive bone degradation and facilitate prostate cancer colonization Preserves bone integrity and prevents skeletal-related events
Autophagy inhibition Blocks autophagosome-lysosome fusion Tumor cells exploit autophagy for survival in nutrient-deprived bone microenvironments Enhances chemosensitivity and induces apoptotic death
mTOR pathway inhibition Suppresses protein synthesis and cell growth mTOR is hyperactive in aggressive prostate cancer Slows down proliferation and synergizes with other anticancer therapies
Multipathway synergy via nanoform Sustained release, ECM targeting, tumor tropism Improves bioavailability and site-specific activity Overcomes pharmacokinetic limitations of pristine NIC and enhances overall efficacy
AR-V7 degradation Promotes proteasomal degradation of AR splice variant AR-V7 AR-V7 drives resistance to androgen receptor-targeted therapies in CRPC Restores sensitivity to enzalutamide/abiraterone and impairs tumor progression
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Despite these advantages, free niclosamide’s systemic administration is limited by rapid metabolism, gastrointestinal degradation, and nonspecific tissue accumulation.

Nanoengineering Niclosamide for Bone-Targeted Delivery

To maximize therapeutic utility, nanohybrids can be employed to encapsulate niclosamide in carriers that offer: ,−

  • 1.

    Enhanced solubility and systemic stability – via lipid-polymer hybrids or amphiphilic micelles.

  • 2.

    Bone-targeting capability – by conjugation with bisphosphonates, tetracycline derivatives, or hydroxyapatite-binding peptides.

  • 3.

    Controlled and stimuli-responsive release – triggered by acidic tumor microenvironment or enzymatic activity.

  • 4.

    Immunomodulation and microenvironmental remodeling via codelivery with immune adjuvants or bone niche inhibitors.

Recent work with layered double hydroxides (LDHs), polymeric nanogels, and mesoporous silica nanoparticles has shown promise and is effective in facilitating sustained niclosamide delivery to metastatic niches.

Translational Prospects and Future Directions

The clinical translation of nano-NIC for advanced prostate cancer with bone metastasis necessitates comprehensive validation in physiologically relevant models. Preclinical studies using intratibial injections and spontaneous bone metastasis from orthotopic prostate tumor models will be critical to assess therapeutic efficacy and skeletal targeting. Advanced imaging modalities such as PET/CT, along with bone turnover biomarkers and patient-derived xenografts (PDX), can elucidate NIC’s biodistribution, ECM engagement, and antimetastatic performance in vivo.

Nano-NIC’s ability to modulate the tumor microenvironmentvia inhibition of EMT, suppression of pro-inflammatory cytokines (IL-1β, IL-6, TNFα), and downregulation of key signaling pathways (STAT3, TGF-β, mTOR/mTORC1, and Wnt/β-catenin)positions it as a promising candidate to disrupt the metastatic cascade and osteoclast-mediated bone colonization in prostate cancer. This targeted approach addresses a major clinical challenge: skeletal-related events that compromise patient outcomes in late-stage diseases (Figure ).

1.

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Schematic illustration of the therapeutic mechanisms of nano-NIC in advanced prostate cancer with bone metastasis, highlighting enhanced ECM-targeting and improved efficacy. The nano-NIC, optimized for size, surface charge, and bioavailability, demonstrates efficient systemic circulation and preferential accumulation within the prostate tumor microenvironment (TME). This facilitates superior interaction with extracellular matrix (ECM) components, promoting ECM remodeling and alleviating stromal barriers to drug penetration. In the context of prostate cancer, nano-NIC disrupts epithelial–mesenchymal transition (EMT) and metastatic signaling by suppressing key pro-inflammatory cytokines (IL-1β, IL-6, TNFα) and inhibiting STAT3 and TGF-β signaling pathways, thereby reducing the activation of cancer-associated fibroblasts (CAFs). Furthermore, it downregulates the mTOR/mTORC1 and Wnt/β-catenin pathways, which are critical for prostate cancer cell proliferation, stemness, and metabolic adaptation. Importantly, nano-NIC inhibits osteoclastogenesis and interferes with the vicious cycle of bone metastasis, providing protection against skeletal colonizationa major complication in advanced prostate cancer. In contrast, unformulated (pristine) NIC exhibits a poor systemic bioavailability and limited therapeutic action. This schematic underscores how nanohybrid transforms NIC into a potent, multifunctional agent with enhanced distribution, ECM modulation, and targeted antimetastatic efficacy in bone-invading prostate cancer. (The image was created using Biorender.com).

Moreover, the therapeutic scope of NIC-loaded nanocarriers could be expanded to other cancers prone to bone dissemination such as breast and pancreatic cancers. Key to clinical adoption will be formulation scalability, GMP-compliant manufacturing, and strategic incorporation into current treatment protocols, including combinations with standard-of-care agents such as docetaxel or radiopharmaceuticals such as radium-223.

Niclosamide has already been evaluated in clinical trials, where oral doses of up to 4800 mg/day (1600 mg three times daily) were well tolerated without dose-limiting toxicities. Notably, in a Phase Ib trial involving patients with castration-resistant prostate cancer, niclosamide demonstrated favorable safety and achieved complete prostate-specific antigen (PSA) responses in some patients when combined with abiraterone and prednisone. These findings highlight the clinical potential of niclosamide as a viable therapeutic agent for prostate cancer, particularly in resistant disease settings.

The clinical challenge posed by advanced prostate cancer with skeletal metastasis highlights a critical gap in effective bone-targeted therapies. Nanoengineered niclosamide (nano-NIC) presents a scientifically compelling and translationally viable strategy to inhibit both primary tumor growth and metastatic progression by modulating multiple oncogenic pathways. As precision nanomedicine continues to evolve, such approaches have the potential to transform the therapeutic landscape for metastatic prostate cancer and other osteotropic malignancies.

Acknowledgments

This study was supported by National Research Foundation of Korea (NRF) grants (No. RS-2023-00245466 and RS-2023-00242339).

All the data associated with this article are available in the present manuscript.

All authors contributed to the conceptualization, drafting, and critical revision of this perspective.

The authors declare no competing financial interest.

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Data Availability Statement

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