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The Tyrosine Kinase Inhibitor Imatinib Mesylate Enhances the Efficacy of Photodynamic Therapy by Inhibiting ABCG2
Open accessAbstract
Purpose: The ATP-binding cassette protein ABCG2 (breast cancer resistance protein) effluxes some of the photosensitizers used in photodynamic therapy (PDT) and, thus, may confer resistance to this treatment modality. Tyrosine kinase inhibitors (TKI) can block the function of ABCG2. Therefore, we tested the effects of the TKI imatinib mesylate (Gleevec) on photosensitizer accumulation and in vitro and in vivo PDT efficacy. Experimental Design: Energy-dependent photosensitizer efflux and imatinib mesylate's effects on intracellular accumulation of clinically used second- and first-generation photosensitizers were studied by flow cytometry in murine and human cells with and without ABCG2 expression. Effects of ABCG2 inhibition on PDT were examined in vitro using cell viability assays and in vivo measuring photosensitizer accumulation and time to regrowth in a RIF-1 tumor model. Results: Energy-dependent efflux of 2-(1-hexyloxethyl)-2-devinyl pyropheophorbide-a (HPPH, Photochlor), endogenous protoporphyrin IX (PpIX) synthesized from 5-aminolevulenic acid, and the benzoporphyrin derivative monoacid ring A (BPD-MA, Verteporfin) was shown in ABCG2+ cell lines, but the first-generation multimeric photosensitizer porfimer sodium (Photofrin) and a novel derivative of HPPH conjugated to galactose were minimally transported. Imatinib mesylate increased accumulation of HPPH, PpIX, and BPD-MA from 1.3- to 6-fold in ABCG2+ cells, but not in ABCG2− cells, and enhanced PDT efficacy both in vitro and in vivo. Conclusions: Second-generation clinical photosensitizers are transported out of cells by ABCG2, and this effect can be abrogated by coadministration of imatinib mesylate. By increasing intracellular photosensitizer levels in ABCG2+ tumors, imatinib mesylate or other ABCG2 transport inhibitors may enhance efficacy and selectivity of clinical PDT.
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“Protein kinase inhibitors are suggested to potentially enhance the PDD efficacy by blocking ABCG2-mediated porphyrin efflux from cancer cells.”
In the citing paper
“Imatinib is the first kinase inhibitor shown to increase ALA-PpIX fluorescence and PDT in tumor cell lines through its interaction with ABCG2 [134].”
From 5-Aminolevulinic Acid as a Theranostic Agent for Tumor Fluorescence Imaging and Photodynamic Therapy (2023) · cites this paper as [134]
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Metadata
- Authors
- Liu, W., Baer, M. R., Bowman, M. J., Pera, P., Zheng, X., Morgan, J., Pandey, R. A., & Oseroff, A. R.
- Affiliations
- 1Dermatology, Departments of
- 2Medicine, and
- Roswell Park Comprehensive Cancer Center (US)
- Venue
- Clinical Cancer Research
- Published
- 2007-04-15
- Volume
- 13
- Issue
- 8
- Pages
- 2463-2470
- ISSN
- 1078-0432 (ISSN-L)
- 1557-3265
- OpenAlex
- W2147445587
- Cited by
- 136
- References
- 47
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 7 · 2023: 9 · 2022: 7 · 2021: 4 · 2020: 6 · 2019: 9 · 2018: 7 · 2017: 7 · 2016: 2 · 2015: 12 · 2014: 13 · 2013: 6 · 2012: 12
- FWCI
- 5.49
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Clinical Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cheng Kung University Hospital
- National Cancer Institute (P30 CA16056, P01 CA55791, P01CA055791, P30CA016056)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Photodynamic Therapy Research Studies
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Physical Sciences › Engineering › Biomedical Engineering › Nanoplatforms for cancer theranostics
- Keywords
- imatinib mesylate, ABCG2, photodynamic therapy, photosensitizer accumulation, tyrosine kinase inhibitors, drug resistance, HPPH, protoporphyrin IX, verteporfin, porfimer sodium, combination therapy
- MeSH terms
- Imatinib Mesylate, ATP Binding Cassette Transporter, Subfamily G, Member 2, Antineoplastic Agents, Benzamides, Carcinoma, Squamous Cell, Combined Modality Therapy, Humans, Hypopharyngeal Neoplasms, Neoplasm Proteins, Photochemotherapy, Piperazines, Protein-Tyrosine Kinases, Pyrimidines, Photosensitizing Agents, ATP-Binding Cassette Transporters, Cell Line, Tumor
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