ArticleCancer cell2010
Sp1/NFkappaB/HDAC/miR-29b regulatory network in KIT-driven myeloid leukemia.
Article in Cancer cell, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT01927354 (Observational Study on the Investigation of the Molecular Mechanism and Clinical Significance of the Interplay Between Twist1 and Other EMT Regulators Through microRNA-29 Family.), which is not on this map. Cited by 161 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Observational Study on the Investigation of the Molecular Mechanism and Clinical Significance of the Interplay Between Twist1 and Other EMT Regulators Through microRNA-29 Family.
Who cites it
161 citing papers in PubMed, 244 citations in OpenAlex.
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- Clinical and pharmacodynamic activity of bortezomib and decitabine in acute myeloid leukemia.Blood · 2012Trial
- A Comprehensive Guide on Epigenetics' Precision Role in Uncommon "Rare" Cancers' Biology and Treatment Frontiers.Sub-cellular biochemistry · 2026Review
- Functions, mechanisms, and therapeutic implications of noncoding RNA in acute myeloid leukemia.Fundamental research · 2025Review
- An unfolded protein response (UPR)-signature regulated by the NFKB-miR-29b/c axis fosters tumor aggressiveness and poor survival in bladder cancer.Frontiers in molecular biosciences · 2025Article
- Dasatinib in core-binding factor acute myeloid leukemia: A promising therapeutic approach.EJHaem · 2024Article
- Bortezomib suppresses acute myelogenous leukaemia stem-like KG-1a cells via NF-κB inhibition and the induction of oxidative stress.Journal of cellular and molecular medicine · 2024Article
- NCAPD3 exerts tumor-promoting effects in prostatic cancer via dual impact on miR-30a-5p by STAT3-MALAT1 and MYC.Cell death discovery · 2024Article
- Combination of eriocalyxin B and homoharringtonine exerts synergistic anti-tumor effects against t(8;21) AML.Acta pharmacologica Sinica · 2024Article
- A novel therapeutic strategy: the significance of exosomal miRNAs in acute myeloid leukemia.Medical oncology (Northwood, London, England) · 2024Review
- High glucose impairs cognitive function through inducing mitochondrial calcium overload in Treg cells.iScience · 2024Article
- Evaluation of MicroRNA as Minimal Residual Disease in Leukemia: Diagnostic and Prognostic Approach: A Review.Iranian journal of public health · 2023Review
- MicroRNA-Mediated Regulation of Histone-Modifying Enzymes in Cancer: Mechanisms and Therapeutic Implications.Biomolecules · 2023Review
- Article
- Preclinical development and evaluation of nanobody-based CD70-specific CAR T cells for the treatment of acute myeloid leukemia.Cancer immunology, immunotherapy : CII · 2023Article
- Specificity Proteins (Sp) and Cancer.International journal of molecular sciences · 2023Review
- NF-κB: A Druggable Target in Acute Myeloid Leukemia.Cancers · 2022Review
- An Assessment on Ethanol-Blended Gasoline/Diesel Fuels on Cancer Risk and Mortality.International journal of environmental research and public health · 2021Review
101 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
27 authors at 2 institutions in 2 countries.
Funding
Abstract
The biologic and clinical significance of KIT overexpression that associates with KIT gain-of-function mutations occurring in subsets of acute myeloid leukemia (AML) (i.e., core binding factor AML) is unknown. Here, we show that KIT mutations lead to MYC-dependent miR-29b repression and increased levels of the miR-29b target Sp1 in KIT-driven leukemia. Sp1 enhances its own expression by participating in a NFkappaB/HDAC complex that further represses miR-29b transcription. Upregulated Sp1 then binds NFkappaB and transactivates KIT. Therefore, activated KIT ultimately induces its own transcription. Our results provide evidence that the mechanisms of Sp1/NFkappaB/HDAC/miR-29b-dependent KIT overexpression contribute to leukemia growth and can be successfully targeted by pharmacological disruption of the Sp1/NFkappaB/HDAC complex or synthetic miR-29b treatment in KIT-driven AML.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.