ArticleBlood2015
Overexpression and knockout of miR-126 both promote leukemogenesis.
Article in Blood, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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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.
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Who cites it
61 citing papers in PubMed, 135 citations in OpenAlex.
- Emerging role of RNA modification reader YTHDF2 in hematopoiesis, immunity, and cancer.MedScience · 2026Review
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- Unveiling the role of microRNAs, the PI3K/AKT pathway, and their associations in various types of leukemia: a comprehensive review.Blood research · 2025Review
- The roles of non-coding RNAs (ncRNAs) in the function of leukemic stem cells (LSCs): a comprehensive review.Discover oncology · 2025Review
- The paradox of hnRNPK: both absence and excess impair skeletal muscle function in mice.Skeletal muscle · 2025Article
- Role of MicroRNAs in Acute Myeloid Leukemia.Genes · 2025Review
- Structural insights into a highly flexible zinc finger module unravel INSM1 function in transcription regulation.Nature communications · 2025Article
- Non-coding RNAs as therapeutic targets in cancer and its clinical application.Journal of pharmaceutical analysis · 2024Review
- Targeting PRMT9-mediated arginine methylation suppresses cancer stem cell maintenance and elicits cGAS-mediated anticancer immunity.Nature cancer · 2024Article
- Low expression of miR-182 caused by DNA hypermethylation accelerates acute lymphocyte leukemia development by targeting PBX3 and BCL2: miR-182 promoter methylation is a predictive marker for hypomethylation agents + BCL2 inhibitor venetoclax.Clinical epigenetics · 2024Article
- Low-dose hypomethylating agents cooperate with ferroptosis inducers to enhance ferroptosis by regulating the DNA methylation-mediated MAGEA6-AMPK-SLC7A11-GPX4 signaling pathway in acute myeloid leukemia.Experimental hematology & oncology · 2024Article
- MicroRNAs Associated with a Bad Prognosis in Acute Myeloid Leukemia and Their Impact on Macrophage Polarization.Biomedicines · 2024Review
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- RNA mGenes & diseases · 2024Article
- miR-126 identifies a quiescent and chemo-resistant human B-ALL cell subset that correlates with minimal residual disease.Leukemia · 2023Article
- Circulating cardiac MicroRNAs safeguard against dilated cardiomyopathy.Clinical and translational medicine · 2023Article
- Epigenetic regulation in hematopoiesis and its implications in the targeted therapy of hematologic malignancies.Signal transduction and targeted therapy · 2023Review
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- Article
- Platelet-Derived miR-126-3p Directly Targets AKT2 and Exerts Anti-Tumor Effects in Breast Cancer Cells: Further Insights in Platelet-Cancer Interplay.International journal of molecular sciences · 2022Article
1 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
25 authors at 8 institutions in 2 countries.
Funding
Abstract
It is generally assumed that gain- and loss-of-function manipulations of a functionally important gene should lead to the opposite phenotypes. We show in this study that both overexpression and knockout of microRNA (miR)-126 surprisingly result in enhanced leukemogenesis in cooperation with the t(8;21) fusion genes AML1-ETO/RUNX1-RUNX1T1 and AML1-ETO9a (a potent oncogenic isoform of AML1-ETO). In accordance with our observation that increased expression of miR-126 is associated with unfavorable survival in patients with t(8;21) acute myeloid leukemia (AML), we show that miR-126 overexpression exhibits a stronger effect on long-term survival and progression of AML1-ETO9a-mediated leukemia stem cells/leukemia initiating cells (LSCs/LICs) in mice than does miR-126 knockout. Furthermore, miR-126 knockout substantially enhances responsiveness of leukemia cells to standard chemotherapy. Mechanistically, miR-126 overexpression activates genes that are highly expressed in LSCs/LICs and/or primitive hematopoietic stem/progenitor cells, likely through targeting ERRFI1 and SPRED1, whereas miR-126 knockout activates genes that are highly expressed in committed, more differentiated hematopoietic progenitor cells, presumably through inducing FZD7 expression. Our data demonstrate that miR-126 plays a critical but 2-faceted role in leukemia and thereby uncover a new layer of miRNA regulation in cancer. Moreover, because miR-126 depletion can sensitize AML cells to standard chemotherapy, our data also suggest that miR-126 represents a promising therapeutic target.
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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.