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ORIGINAL RESEARCH

MIL-88A@catechin as a dual-action therapeutic for reactive oxygen species-mediated apoptosis and angiogenesis modulation in breast cancer in vitro and in vivo

Soheil Sojdeh1,2 ,  Mojtaba Bagherzadeh1* ,  Maryam Ahmadifar3 ,  Majid Salehi4 ,  Hossein Daneshgar1 ,  Mostafa Pourfallah5 ,  Mohammad Edrisi6 ,  Navid Rabiee7,8,9,10
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1 Department of Inorganic Chemistry, Faculty of Chemistry, Sharif University of Technology, Tehran, Iran
2 Department of Ophthalmology and Visual Science, College of Medicine, University of Illinois, Chicago, Illinois, United States of America
3 Department of Chemistry, Faculty of Science, K.N. Toosi University of Technology, Tehran, Iran
4 Department of Tissue Engineering, School of Medicine, Shahroud University of Medical Sciences, Shahroud, Semnan, Iran
5 Department of Cell and Molecular Sciences, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran
6 Institute of Biochemistry and Biophysics, University of Tehran, Tehran, Iran
7 Department of Biomaterials, Saveetha Dental College and Hospitals, SIMATS, Saveetha University, Chennai, India
8 Department of Basic Medical Science, School of Medicine, Tsinghua University, Beijing, China
9 Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing, China
10 MOE Key Laboratory of Bioinformatics, Tsinghua University, Beijing, China
BMT, 24 https://doi.org/10.12336/bmt.26.00024
Submitted: 3 February 2026 | Revised: 11 March 2026 | Accepted: 11 March 2026 | Published: 20 May 2026
© 2026 by the Author(s). Licensee Biomaterials Translational, USA. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 (CC BY-NC-SA 4.0) (https://creativecommons.org/licenses/by-nc-sa/4.0/deed.en)
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Abstract

Breast cancer continues to pose a significant clinical challenge due to its fast progression and resistance to therapy, requiring novel treatment approaches. We present the design and assessment of a defective iron-based metal–organic framework (MIL-88A) functionalized with catechin (MIL-88A@catechin) as a dual-action platform for redox regulation and targeted cancer treatment. The defect-engineered MIL-88A framework, containing approximately 0.6148 missing linkers per Fe3 node, was confirmed by CHN elemental analysis and inductively coupled plasma mass spectrometry. These structural defects create stable coordination sites that facilitate catechin immobilization through iron–phenolate interactions. The redox activity of MIL-88A@catechin was shown by increased reactive oxygen species production by catechin-facilitated Fe3+/Fe2+ cycling, while structural characterization was confirmed by Fourier transform infrared spectroscopy, X-ray diffraction, thermogravimetric analysis, field-emission scanning electron microscopy, and X-ray photoelectron spectroscopy. In vitro investigations revealed preferential cytotoxicity against MDA-MB-231 breast cancer cells (IC50 = 25.16 μg/mL), while preserving over 80% viability in normal MCF-10A cells. Flow cytometry indicated 17.7% early apoptosis, 21.3% late apoptosis, and 4.38% necrosis, affirming apoptosis as the predominant mechanism. Quantitative reverse transcription polymerase chain reaction analysis demonstrated a considerable overexpression of BAX (p<0.01), CASP9 (p<0.001), and CASP8 (p<0.0001), in conjunction with elevated BCL2 expression (p<0.0001), indicating the activation of both intrinsic and extrinsic apoptotic pathways. In vivo assessment in a mouse breast cancer model revealed decreased tumor necrosis (50–60% compared to 60–70% in controls), lower mitotic counts (31 vs. 37), and increased apoptotic cell numbers (10 vs. 7). Gene expression analysis demonstrated the downregulation of CASP8 (p<0.05) and VEGFR2 (p<0.01), with the overexpression of CASP9 (p<0.001) and VEGFR1 (p<0.001), underscoring intrinsic apoptotic activation and angiogenesis modulation.

Keywords
MIL-88A@catechin
Reactive oxygen species-mediated apoptosis
Angiogenesis modulation
Breast cancer therapy
Funding
None.
Conflict of interest
The authors declare no conflicts of interest.
References
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