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Efficient intervention of growth and infiltration of primary adult T-cell leukemia cells by an HIV protease inhibitor, ritonavir
Open accessAbstract
Adult T-cell leukemia (ATL), an aggressive malignancy of CD4+ T cells associated with human T-cell leukemia virus type I (HTLV-I) infection, carries a very poor prognosis because of the resistance of leukemic cells to any conventional regimen, including chemotherapy. We examined the effect of ritonavir, an HIV protease inhibitor, on HTLV-I-infected T-cell lines and primary ATL cells and found that it induced apoptosis and inhibited transcriptional activation of NF-kappaB in these cells. Furthermore, ritonavir inhibited expression of Bcl-xL, survivin, c-Myc, and cyclin D2, the targets of NF-kappaB. In nonobese diabetic/severe combined immunodeficient (NOD/SCID)/gammacnull (NOG) mice, ritonavir very efficiently prevented tumor growth and leukemic infiltration in various organs of NOG mice at the same dose used for treatment of patients with AIDS. Our data indicate that ritonavir has potent anti-NF-kappaB and antitumor effects and might be clinically applicable for treatment of ATL. These results would provide a new concept and novel platform for new drug development of leukemia and solid cancer as well.
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Ritonavir displayed anti-leukaemic activity against ATL cells ex vivo, mostly due to inhibitory effects on the NF-κB target rather than PR.
“The most notable of the FDA-approved PR inhibitors to be applied in the treatment of HTLV-1 is ritonavir, which did display anti-leukaemic activity against ATL cells ex vivo; however, this was mostly due to the inhibitory effects exerted on the NF-κB target rather than PR [190].”
From Current State of Therapeutics for HTLV-1 (2024) · cites this paper as [190]
The Results (p. 4) report reduced survival and increased apoptosis of freshly isolated ATL cells after ritonavir treatment. The Discussion (p. 7) links anti-ATL activity to suppression of NF-κB, but says ritonavir’s activity against HTLV-I protease was not assessed and a direct antiviral effect could not be ruled out. It therefore does not establish that NF-κB inhibition was the predominant mechanism rather than protease inhibition. (LLM, conf=0.88)
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References 59 · Cited by 75
Metadata
- Authors
- Dewan, M. Z.
- Affiliations
- Kagoshima University (JP)
- Corresponding author
- Dewan, M. Z.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2006-01-15
- Volume
- 107
- Issue
- 2
- Pages
- 716-724
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2163653305
- Cited by
- 75
- References
- 59
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 3 · 2022: 3 · 2021: 5 · 2020: 5 · 2019: 1 · 2018: 2 · 2015: 4 · 2014: 2 · 2013: 3 · 2012: 2
- FWCI
- 2.61
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Blood (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Health Sciences › Medicine › Oncology › Viral-associated cancers and disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- adult T-cell leukemia/lymphoma, ritonavir, HIV protease inhibitors, HTLV-1, NF-κB, apoptosis, Bcl-xL, survivin, c-Myc, cyclin D2, tumor growth inhibition, leukemic infiltration, NOG mice, CD4+ T cells
- MeSH terms
- Survivin, Adult, Aged, Aged, 80 and over, Animals, Disease Models, Animal, Female, Humans, Male, Microtubule-Associated Proteins, Middle Aged, Neoplasm Proteins, Neoplasms, Experimental, Transcription, Genetic, Human T-lymphotropic virus 1, Leukemia-Lymphoma, Adult T-Cell, Cyclins, Proto-Oncogene Proteins c-myc, NF-kappa B, Mice, SCID, Mice, Inbred NOD, Apoptosis, HIV Protease Inhibitors, Ritonavir, bcl-X Protein, Inhibitor of Apoptosis Proteins, Mice, Cyclin D2
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