ArticleLeukemia2022
The tumor suppressor MIR139 is silenced by POLR2M to promote AML oncogenesis.
Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- Differential Expression and Target Gene Analysis of PBMC-Derived microRNAs as Prognostic Biomarkers in Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2026Article
- Unveiling histotype-specific biomarkers in ovarian carcinoma using proteomics.Molecular therapy. Oncology · 2025Article
- Partners in Silencing: Decoding the Mammalian Argonaute Interactome.Non-coding RNA · 2025Review
- Forced exercise modulates retinal inflammatory response and regulates miRNA expression to promote retinal neuroprotection during degeneration.bioRxiv : the preprint server for biology · 2025Article
- Review
- Crosstalk between Noncoding RNAs and the Epigenetics Machinery in Pediatric Tumors and Their Microenvironment.Cancers · 2023Review
- Human circulating small non-coding RNA signature as a non-invasive biomarker in clinical diagnosis of acute myeloid leukaemia.Theranostics · 2023Article
- Article
- Review
- Potential of the miR-200 Family as a Target for Developing Anti-Cancer Therapeutics.International journal of molecular sciences · 2022Review
- Review
- miR-139-3p/Kinesin family member 18B axis suppresses malignant progression of gastric cancer.Bioengineered · 2022Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MIR139 is a tumor suppressor and is commonly silenced in acute myeloid leukemia (AML). However, the tumor-suppressing activities of miR-139 and molecular mechanisms of MIR139-silencing remain largely unknown. Here, we studied the poorly prognostic MLL-AF9 fusion protein-expressing AML. We show that MLL-AF9 expression in hematopoietic precursors caused epigenetic silencing of MIR139, whereas overexpression of MIR139 inhibited in vitro and in vivo AML outgrowth. We identified novel miR-139 targets that mediate the tumor-suppressing activities of miR-139 in MLL-AF9 AML. We revealed that two enhancer regions control MIR139 expression and found that the polycomb repressive complex 2 (PRC2) downstream of MLL-AF9 epigenetically silenced MIR139 in AML. Finally, a genome-wide CRISPR-Cas9 knockout screen revealed RNA Polymerase 2 Subunit M (POLR2M) as a novel MIR139-regulatory factor. Our findings elucidate the molecular control of tumor suppressor MIR139 and reveal a role for POLR2M in the MIR139-silencing mechanism, downstream of MLL-AF9 and PRC2 in AML. In addition, we confirmed these findings in human AML cell lines with different oncogenic aberrations, suggesting that this is a more common oncogenic mechanism in AML. Our results may pave the way for new targeted therapy in AML.
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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.