Transcription intermediary factor 1γ is a tumor suppressor in mouse and human chronic myelomonocytic leukemia
Open accessAbstract
Transcription intermediary factor 1γ (TIF1γ) was suggested to play a role in erythropoiesis. However, how TIF1γ regulates the development of different blood cell lineages and whether TIF1γ is involved in human hematological malignancies remain to be determined. Here we have shown that TIF1γ was a tumor suppressor in mouse and human chronic myelomonocytic leukemia (CMML). Loss of Tif1g in mouse HSCs favored the expansion of the granulo-monocytic progenitor compartment. Furthermore, Tif1g deletion induced the age-dependent appearance of a cell-autonomous myeloproliferative disorder in mice that recapitulated essential characteristics of human CMML. TIF1γ was almost undetectable in leukemic cells of 35% of CMML patients. This downregulation was related to the hypermethylation of CpG sequences and specific histone modifications in the gene promoter. A demethylating agent restored the normal epigenetic status of the TIF1G promoter in human cells, which correlated with a reestablishment of TIF1γ expression. Together, these results demonstrate that TIF1G is an epigenetically regulated tumor suppressor gene in hematopoietic cells and suggest that changes in TIF1γ expression may be a biomarker of response to demethylating agents in CMML.
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Trim33−/− mice have been shown to develop chronic myelomonocytic leukemia.
“Trim33−/− mice have been shown to develop chronic myelomonocytic leukemia (Aucagne et al., 2011)”
From The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer (2015) · cites this paper as Aucagne et al., 2011
The research article (p. 2) and Figure 3 (p. 4) report that Tif1g-deficient mice older than six months develop a CMML-like myeloproliferative disease. The claim captures the disease resemblance but omits the age qualifier and calls it CMML rather than CMML-like. (LLM, conf=0.88)
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Wang, E., Kawaoka, S., Roe, J.-S., Shi, J., Hohmann, A. F., Xu, Y., Bhagwat, A. S., Suzuki, Y., Kinney, J. B., & Vakoc, C. R. (2015) · eLife · doi:10.7554/elife.06377 · Cited by 54 · see citing works
“However, we observe a modest expansion of myeloid cells upon short durations of TRIM33 suppression in vivo and Trim33−/− mice have been shown to develop chronic myelomonocytic leukemia (Aucagne et al., 2011).”
BackgroundResultInfluential
- Authors
- Aucagne, R., Droin, N., Paggetti, J., Lagrange, B., Largeot, A., Hammann, A., Bataille, A., Martin, L., Yan, K.-P., Fenaux, P., Losson, R., Solary, E., Bastie, J.-N., & Delva, L.
- Affiliations
- Inserm (FR)
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2011-06-01
- Volume
- 121
- Issue
- 6
- Pages
- 2361-2370
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC3104753
- OpenAlex
- W2107148940
- Cited by
- 117
- References
- 63
- Citations by year
- 2026: 3 · 2025: 2 · 2024: 10 · 2023: 4 · 2022: 3 · 2021: 8 · 2020: 6 · 2019: 8 · 2018: 5 · 2017: 13 · 2016: 4 · 2015: 12 · 2014: 10 · 2013: 9 · 2012: 12
- FWCI
- 8.53
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- univOAK (4 institutions : Université de Strasbourg, Université de Haute Alsace, INSA Strasbourg, Bibliothèque Nationale et Universitaire de Strasbourg) (submittedVersion)
- Funders
- Association pour la Recherche sur le Cancer
- Agence Nationale de la Recherche
- Institut National de la Santé et de la Recherche Médicale
- Ligue Contre le Cancer
- Fondation de France
- Université de Bourgogne
- Ministère de l'Enseignement Supérieur et de la Recherche
- Institut National Du Cancer
- Institut Gustave-Roussy
- Conseil régional de Bourgogne-Franche-Comté
- Société Française d'Hématologie
- Topics
- Health Sciences › Medicine › Hematology › Acute Myeloid Leukemia Research
- Health Sciences › Medicine › Genetics › Myeloproliferative Neoplasms: Diagnosis and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- TIF1γ, chronic myelomonocytic leukemia, tumor suppressor, epigenetic regulation, DNA methylation, CpG hypermethylation, histone modifications, hypomethylating agents, hematopoietic stem cells, myeloproliferative neoplasms
- MeSH terms
- Decitabine, Aged, Aged, 80 and over, Aging, Animals, Antimetabolites, Antineoplastic, Azacitidine, Base Sequence, Cell Differentiation, Female, Hematopoiesis, Hematopoietic Stem Cells, Humans, Male, Middle Aged, Molecular Sequence Data, Neoplasm Proteins, Promoter Regions, Genetic, Specific Pathogen-Free Organisms, Transcription Factors, Leukemia, Myelomonocytic, Chronic, Gene Expression Regulation, Leukemic, Genes, Tumor Suppressor, Receptor, Macrophage Colony-Stimulating Factor, Mice, Knockout, DNA Methylation, Mice
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