ArticleInternational journal of hematology2012
Down-regulation of hematopoiesis master regulator PU.1 via aberrant methylation in chronic myeloid leukemia.
Article in International journal of hematology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 25 citations in OpenAlex.
- Targeting DNA Methylation in Leukemia, Myelodysplastic Syndrome, and Lymphoma: A Potential Diagnostic, Prognostic, and Therapeutic Tool.International journal of molecular sciences · 2022Review
- Comprehensive Analysis of Immune Implications and Prognostic Value of SPI1 in Gastric Cancer.Frontiers in oncology · 2022Article
- Review
- Inflammation as a regulator of hematopoietic stem cell function in disease, aging, and clonal selection.The Journal of experimental medicine · 2021Review
- PU.1 enforces quiescence and limits hematopoietic stem cell expansion during inflammatory stress.The Journal of experimental medicine · 2021Article
- Article
- BCR-ABL1 mediated miR-150 downregulation through MYC contributed to myeloid differentiation block and drug resistance in chronic myeloid leukemia.Haematologica · 2018Article
- Transcriptional regulation of the proto-oncogene Zfp521 by SPI1 (PU.1) and HOXC13.Genesis (New York, N.Y. : 2000) · 2016Article
- Epigenetic roots of immunologic disease and new methods for examining chromatin regulatory pathways.Immunology and cell biology · 2015Review
- CITED2-mediated human hematopoietic stem cell maintenance is critical for acute myeloid leukemia.Leukemia · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The PU.1 transcription factor is a crucial regulator of hematopoiesis, and its expression is altered in various leukemic processes. It has been shown that expression of PU.1 is severely impaired in patients with chronic myeloid leukemia (CML), but the mechanism underlying this effect remains unknown. Through bisulfite sequencing, semi-quantitative PCR, and indirect immunofluorescence and Western blot techniques, we found aberrant methylation in the promoter region of transcription factor PU.1 in CML patients both in the chronic and blast crisis phases, as well as in the CML blast K562 cell line. Of these, several CpG sites were more highly methylated in blast crisis than chronic phase, while no methylation of these sites was observed in healthy individuals. Interestingly, CML patients achieved complete cytogenetic remission under imatinib mesylate treatment, but the aberrant methylation status of PU.1 was not reversed. Down-regulation of PU.1 expression at the mRNA and protein levels was also observed in association with aberrant methylation. Thus, for the first time, we have revealed a potential epigenetic modification of PU.1 in CML, which may be responsible for the down-regulation of PU.1. These data suggest that aberrant methylation of PU.1 may play a role in CML pathogenesis, and may therefore serve as a useful biomarker and potential target for demethylating drugs.
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