The Novel Anticancer Agent JNJ-26854165 Induces Cell Death through Inhibition of Cholesterol Transport and Degradation of ABCA1
Open accessAbstract
JNJ-26854165 (serdemetan) has previously been reported to inhibit the function of the E3 ligase human double minute 2, and we initially sought to characterize its activity in models of mantle cell lymphoma (MCL) and multiple myeloma (MM). Serdemetan induced a dose-dependent inhibition of proliferation in both wild-type (wt) and mutant (mut) p53 cell lines, with IC50 values from 0.25 to 3 μM/l, in association with an S phase cell cycle arrest. Caspase-3 activation was primarily seen in wtp53-bearing cells but also occurred in mutp53-bearing cells, albeit to a lesser extent. 293T cells treated with JNJ-26854165 and serdemetan-resistant fibroblasts displayed accumulation of cholesterol within endosomes, a phenotype reminiscent of that seen in the ATP-binding cassette subfamily A member-1 (ABCA1) cholesterol transport disorder, Tangiers disease. MM and MCL cells had decreased cholesterol efflux and electron microscopy demonstrated the accumulation of lipid whorls, confirming the lysosomal storage disease phenotype. JNJ-26854165 induced induction of cholesterol regulatory genes, sterol regulatory element-binding transcription factor-1 and -2, liver X receptors α and β, along with increased expression of Niemann-Pick disease type-C1 and -C2. However, JNJ-26854165 induced enhanced ABCA1 turnover despite enhancing transcription. Finally, ABCA1 depletion resulted in enhanced sensitivity to JNJ-26854165. Overall, these findings support the hypothesis that serdemetan functions in part by inhibiting cholesterol transport and that this pathway is a potential new target for the treatment of MCL and MM.
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JNJ-26854165 (141), also known as serdemetan, is an orally bioavailable compound that blocks the binding of the MDM2-p53 complex to the proteasome and inhibits the degradation of p53, thereby restoring p53-mediated apoptosis of tumor cells.
“JNJ-26854165 (141), also known as serdemetan, is an orally bioavailable compound that blocks the binding of the MDM2-p53 complex to the proteasome and inhibits the degradation of p53, thereby restoring p53-mediated apoptosis of tumor cells.372”
From Recent advances in targeting the “undruggable” proteins: from drug discovery to clinical trials (2023) · cites this paper as [372]
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- Authors
- Jones, R. J., Gu, D., Bjorklund, C. C., Kuiatse, I., Remaley, A. T., Bashir, T., Vreys, V., & Orlowski, R. Z.
- Affiliations
- The University of Texas MD Anderson Cancer Center (US)
- National Institutes of Health (US)
- Venue
- The Journal of Pharmacology and Experimental Therapeutics
- Publisher
- Elsevier BV
- Published
- 2013-09
- Volume
- 346
- Issue
- 3
- Pages
- 381-392
- ISSN
- 0022-3565 (ISSN-L)
- PMC
- PMC3876782
- OpenAlex
- W2110613632
- Cited by
- 26
- References
- 50
- Citations by year
- 2025: 1 · 2024: 2 · 2023: 2 · 2022: 2 · 2021: 3 · 2020: 1 · 2019: 4 · 2018: 2 · 2016: 1 · 2015: 7 · 2014: 1
- FWCI
- 3.29
- Type
- journal article
- Language
- en
- Update notices
- erratum (2013-11-01)
- Open access
- bronze
- doi.org
- Locations
- Journal of Pharmacology and Experimental Therapeutics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- University of Texas MD Anderson Cancer Center (#CA16672)
- National Heart, Lung, and Blood Institute (HL002058-18, Z01HL002058)
- National Cancer Institute (P50CA142509, P30CA016672)
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Lipids, and Metabolism
- Health Sciences › Medicine › Oncology › Drug Transport and Resistance Mechanisms
- Keywords
- ABCA1, cholesterol transport, cholesterol efflux, mantle cell lymphoma, multiple myeloma, p53, caspase-3, lysosomal storage disease, Niemann-Pick disease type C, liver X receptor, anticancer agents, Tangier disease
- MeSH terms
- Animals, Biological Transport, Active, Cell Cycle, Cholesterol, Flow Cytometry, Half-Life, Humans, Microscopy, Electron, Microscopy, Fluorescence, Radiation-Sensitizing Agents, Tryptamines, Blotting, Western, Signal Transduction, Cell Death, ATP-Binding Cassette Transporters, Gene Silencing, Membrane Microdomains, Cell Line, Tumor, Cell Proliferation, Mice, Caspase 3, Real-Time Polymerase Chain Reaction, ATP Binding Cassette Transporter 1
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