ArticleLeukemia research2016
The miR-17∼92 cluster contributes to MLL leukemia through the repression of MEIS1 competitor PKNOX1.
Article in Leukemia research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- The hidden regulators: Non-coding RNAs in KMT2A-rearranged acute lymphoblastic leukemia.International journal of cancer · 2026Review
- Identification of key biomarkers and potential therapeutic drugs in nasopharyngeal carcinoma based on comprehensive bioinformatics analysis.Discover oncology · 2025Article
- Systematic pan-cancer analysis identifies PKNOX1 as a potential prognostic and immunological biomarker and its functional validation.Frontiers in immunology · 2025Article
- The Screening of microRNAs in Chronic Myeloid Leukemia: A Clinical Evaluation.International journal of molecular sciences · 2024Article
- MicroRNAs Associated with a Bad Prognosis in Acute Myeloid Leukemia and Their Impact on Macrophage Polarization.Biomedicines · 2024Review
- Overexpression of miR-17 predicts adverse prognosis and disease recurrence for acute myeloid leukemia.International journal of clinical oncology · 2022Article
- MicroRNAs in Leukemias: A Clinically Annotated Compendium.International journal of molecular sciences · 2022Article
- Non-coding RNAs in cancers with chromosomal rearrangements: the signatures, causes, functions and implications.Journal of molecular cell biology · 2019Review
- MiR-17 family-mediated regulation of Pknox1 influences hepatic steatosis and insulin signaling.Journal of cellular and molecular medicine · 2018Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mixed lineage leukemias have a relatively poor prognosis and arise as a result of translocations between the MLL(KMT2A) gene and one of multiple partner genes. Downstream targets of MLL are aberrantly upregulated and include the developmentally important HOX genes and MEIS1, as well as multiple microRNAs (miRNAs), including the miR-17∼92 cluster. Here we examined the contribution of specific miRNAs to MLL leukemias through knockdown studies utilizing custom anti-microRNA oligonucleotides. Combinatorial treatment against miR-17-5p and miR-19a-3p of the miR-17∼92 cluster dramatically reduces colony forming ability of MLL-fusion containing cell lines relative to non-MLL acute myeloid leukemia (AML) controls. To determine the mechanism by which these miRNAs contribute to leukemia, we validated PKNOX1 as a target of both miR-17-5p and miR-19a-3p. MEIS1 and PKNOX1 are TALE domain proteins that participate in ternary complexes with HOX and PBX partners. Here we establish the competitive relationship between PKNOX1 and MEIS1 in PBX-containing complex formation and determine the antagonistic role of PKNOX1 to leukemia in a murine MLL-AF9 model. These data implicate the miR-17∼92 cluster as part of a regulatory mechanism necessary to maintain MEIS1/HOXA9 -mediated transformation in MLL leukemia, indicating that targeting multiple non-homologous miRNAs may be utilized as a novel therapeutic regimen.
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