ArticleOncogene2016
Deficiency in WT1-targeting microRNA-125a leads to myeloid malignancies and urogenital abnormalities.
Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 17 citations in OpenAlex.
- Micro-RNAs: A safety net to protect hematopoietic stem cell self-renewal.Wiley interdisciplinary reviews. RNA · 2022Review
- Micro-RNA-125a mediates the effects of hypomethylating agents in chronic myelomonocytic leukemia.Clinical epigenetics · 2021Article
- miR-125a-5p regulates megakaryocyte proplatelet formation via the actin-bundling protein L-plastin.Blood · 2020Article
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- Article
- Metazoan MicroRNAs.Cell · 2018Review
- Putative binding sites for mir-125 family miRNAs in the mouse Lfng 3'UTR affect transcript expression in the segmentation clock, but mir-125a-5p is dispensable for normal somitogenesis.Developmental dynamics : an official publication of the American Association of Anatomists · 2017Article
- Pathologically decreased expression of miR-193a contributes to metastasis by targeting WT1-E-cadherin axis in non-small cell lung cancers.Journal of experimental & clinical cancer research : CR · 2016Article
- MicroRNAs in Control of Stem Cells in Normal and Malignant Hematopoiesis.Current stem cell reports · 2016Article
- The roles of microRNAs in the regulation of tumor metastasis.Cell & bioscience · 2015Article
Corrections and comments
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Authors and funding
22 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Wilms' tumor gene WT1 is overexpressed in leukemia and solid tumors and has an oncogenic role in leukemogenesis and tumorigenesis. However, precise regulatory mechanisms of WT1 overexpression remain undetermined. In the present study, microRNA-125a (miR-125a) was identified as a miRNA that suppressed WT1 expression via binding to the WT1-3'UTR. MiR-125a knockout mice overexpressed WT1, developed myeloproliferative disorder (MPD) characterized by expansion of myeloid cells in bone marrow (BM), spleen and peripheral blood, and displayed urogenital abnormalities. Silencing of WT1 expression in hematopoietic stem/progenitor cells of miR-125a knockout MPD mice by short-hairpin RNA inhibited myeloid colony formation in vitro. Furthermore, the incidence and severity of MPD were lower in miR-125a (-/-) mice than in miR-125a (+/-) mice, indicating the operation of compensatory mechanisms for the complete loss of miR-125a. To elucidate the compensatory mechanisms, miRNA array was performed. MiR-486 was occasionally induced in compete loss of miR-125a and inhibited WT1 expression instead of miR-125a, resulting in the cancellation of MPD occurrence. These results showed for the first time the post-transcriptional regulatory mechanisms of WT1 by both miR-125a and miR-486 and should contribute to the elucidation of mechanisms of normal hematopoiesis and kidney development.
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