Expression of Interferon Consensus Sequence Binding Protein (ICSBP) Is Downregulated in Bcr-Abl-Induced Murine Chronic Myelogenous Leukemia-Like Disease, and Forced Coexpression of ICSBP Inhibits Bcr-Abl-Induced Myeloproliferative Disorder
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Chronic myelogenous leukemia (CML) is a clonal myeloproliferative disorder resulting from the neoplastic transformation of a hematopoietic stem cell. The majority of cases of CML are associated with the (9;22) chromosome translocation that generates the bcr-abl chimeric gene. Alpha interferon (IFN-alpha) treatment induces hematological remission and prolongs life in 75% of CML patients in the chronic phase. It has been shown that mice deficient in interferon consensus sequence binding protein (ICSBP), a member of the interferon regulatory factor family, manifest a CML-like syndrome. We have shown that expression of Bcr-Abl in bone marrow (BM) cells from 5-fluorouracil (5-FU)-treated mice by retroviral transduction efficiently induces a myeloproliferative disease in mice resembling human CML. To directly test whether icsbp can function as a tumor suppressor gene, we examined the effect of ICSBP on Bcr-Abl-induced CML-like disease using this murine model for CML. We found that expression of the ICSBP protein was significantly decreased in Bcr-Abl-induced CML-like disease. Forced coexpression of ICSBP inhibited the Bcr-Abl-induced colony formation of BM cells from 5-FU-treated mice in vitro and Bcr-Abl-induced CML-like disease in vivo. Interestingly, coexpression of ICSBP and Bcr-Abl induced a transient B-lymphoproliferative disorder in the murine model of Bcr-Abl-induced CML-like disease. Overexpression of ICSBP consistently promotes rather than inhibits Bcr-Abl-induced B lymphoproliferation in a murine model where BM cells from non-5-FU-treated donors were used, indicating that ICSBP has a specific antitumor activity toward myeloid neoplasms. We also found that overexpression of ICSBP negatively regulated normal hematopoiesis. These data provide direct evidence that ICSBP can act as a tumor suppressor that regulates normal and neoplastic proliferation of hematopoietic cells.
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In the mouse model with a CML-like disease induced by Bcr-Abl, ICSBP expression was downregulated, and the mouse disease was ameliorated by coexpression of ICSBP.
“In the mouse model with a CML-like disease induced by Bcr-Abl, ICSBP expression was also downregulated. Interestingly, the mouse disease was ameliorated by coexpression of ICSBP. (52)”
From Review: ICSBP/IRF-8: Its Regulatory Roles in the Development of Myeloid Cells (2002) · cites this paper as [52]
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- Authors
- Hao, S. X., & Ren, R.
- Affiliations
- Brandeis University (US)
- ORCID
- Ren, Ruibao
- Venue
- Molecular and Cellular Biology
- Publisher
- Informa UK Limited
- Published
- 2000-02-01
- Volume
- 20
- Issue
- 4
- Pages
- 1149-1161
- ISSN
- 0270-7306 (ISSN-L)
- 1098-5549
- PMC
- PMC85233
- OpenAlex
- W2096038076
- Cited by
- 143
- References
- 48
- Citations by year
- 2026: 1 · 2023: 1 · 2021: 5 · 2020: 2 · 2019: 1 · 2018: 2 · 2017: 3 · 2016: 10 · 2015: 6 · 2014: 4 · 2013: 5 · 2012: 6
- FWCI
- 7.42
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular and Cellular Biology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Cancer Institute (CA68008, R01CA068008)
- Topics
- Health Sciences › Medicine › Hematology › Chronic Myeloid Leukemia Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Tyrosine Phosphatases
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Keywords
- IRF8, BCR-ABL, chronic myeloid leukemia, myeloproliferative neoplasms, tumor suppressor, interferon regulatory factors, B-cell lymphoproliferative disorders, hematopoietic regulation, bone marrow cells, retroviral transduction, colony formation
- MeSH terms
- Interferon Regulatory Factor-8, Animals, Antimetabolites, Antineoplastic, B-Lymphocytes, Base Sequence, Colony-Forming Units Assay, Disease Models, Animal, Fluorouracil, Hematopoiesis, Humans, Interferons, Lymphoproliferative Disorders, Male, Mice, Inbred BALB C, Myeloproliferative Disorders, Repressor Proteins, Translocation, Genetic, Leukemia, Myelogenous, Chronic, BCR-ABL Positive, Down-Regulation, Bone Marrow Transplantation, Genes, abl, Consensus Sequence, DNA Primers, Interferon Regulatory Factors, Mice
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