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An In Vitro Dormancy Model of Estrogen-sensitive Breast Cancer in the Bone Marrow: A Tool for Molecular Mechanism Studies and Hypothesis Generation
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Azelastine Inhibits Triple-Negative Breast Cancer Cell Viability via an ARF1-Dependent Mechanism.

Seon Uk Park1, Gi Ung Jung1, Eun Kyung Paik2

  • 1Graduate School of Biomedical Science and Engineering, Hanyang Biomedical Research Institute, College of Medicine, Hanyang University, Seoul 04763, Republic of Korea.

International Journal of Molecular Sciences
|December 30, 2025
PubMed
Summary

Azelastine shows promise for treating triple-negative breast cancer (TNBC) by targeting ADP-ribosylation factor 1 (ARF1), independent of its known H1-antihistamine receptor. This drug repositioning strategy offers a new therapeutic avenue for aggressive TNBC.

Keywords:
ARF1HRH1azelastinecytotoxicitydrug repurposinggolgicide Atriple-negative breast cancer

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Area of Science:

  • Oncology
  • Pharmacology
  • Molecular Biology

Background:

  • Triple-negative breast cancer (TNBC) presents limited therapeutic options due to its aggressive nature and lack of targeted receptors.
  • Azelastine, an H1-antihistamine, is explored for drug repositioning against TNBC.
  • The histamine receptor H1 (HRH1)-independent mechanism of azelastine in TNBC requires elucidation.

Purpose of the Study:

  • To evaluate azelastine's potential for drug repositioning in TNBC.
  • To investigate the HRH1-independent mechanism of azelastine's action in TNBC.
  • To explore the role of ADP-ribosylation factor 1 (ARF1) in azelastine's efficacy.

Main Methods:

  • Cell viability assays (CCK-8) on TNBC cell lines (MDA-MB-231, BT-549) treated with azelastine and desmethyl azelastine.
  • Assessment of HRH1 dependency via histamine stimulation and HRH1 knockdown (siRNA).
  • Investigation of ARF1's role using ARF1 knockdown (siRNA), GBF1 inhibitor (GCA), and Drp1 inhibitor (M-divi 1).

Main Results:

  • Azelastine and desmethyl azelastine significantly reduced TNBC cell viability, with azelastine showing an IC50 of 35.93 µM in MDA-MB-231 cells.
  • Efficacy was HRH1-independent; ARF1 was found to be upregulated in TNBC and crucial for azelastine's action.
  • Azelastine induced Drp1-dependent mitochondrial dysfunction and reduced p-ERK phosphorylation, independent of HRH1.

Conclusions:

  • Azelastine exhibits potent anticancer effects in TNBC cells through an HRH1-independent, ARF1-dependent mechanism.
  • The drug targets the ERK-Drp1 axis and induces mitochondrial dysfunction.
  • This ARF1-dependent pathway supports azelastine's repositioning as a therapeutic agent for ARF1-driven TNBC.