ArticleBlood2021
A critical role of nuclear m6A reader YTHDC1 in leukemogenesis by regulating MCM complex-mediated DNA replication.
Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 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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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.
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Who cites it
107 citing papers in PubMed, 159 citations in OpenAlex.
- A positive feedback loop between YTHDC1 and EP300 drives multiple myeloma tumorigenesis.Oncogene · 2026Article
- AS-TLC-Based High-Throughput Screening Integrated with CuAAC Optimization Strategy Facilitates the Rapid Discovery of YTHDC1 Inhibitor.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Chromosomal rearrangement-enhanced mRNA stability drives the oncogenic potential of fusion genes in pediatric leukemia.Haematologica · 2026Article
- Interplay between the RBP SYNCRIP and RNA methylation in determining sEV miRNA-cargo and function in cell-to-cell communication.Cell death & disease · 2026Article
- The relevance of mJournal of cancer research and clinical oncology · 2026Review
- YTHDC1 recognizes METTL16-dependent mProceedings of the National Academy of Sciences of the United States of America · 2026Article
- m6A Modification of ATOX1 Inhibits Acute Myeloid Leukemia Progression by Promoting Cuproptosis.Cancer research communications · 2026Article
- YTHDC1 Inhibits Esophageal Cancer Cell Apoptosis, Radiosensitivity and Autophagy Via Upregulating PLK1 by Stabilizing USP10.Applied biochemistry and biotechnology · 2026Article
- Low YTHDC1 Expression Upregulates FSCN1 to Promote Nuclear F-Actin Formation and Facilitate Double-strand DNA Breaks Repair in TMZ-Resistant Glioblastoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Domain-derived knowledge enabled machine learning and functional characterization of cancer-associated RNA methylation sites.BMC bioinformatics · 2026Article
- NNature reviews. Cancer · 2026Review
- Nat10-mediated ac4C epitranscriptomics orchestrates hematopoietic stem/progenitor cell fate determination via translation control.Science advances · 2026Article
- Integrative analysis of YTHDC1 phosphoproteome unveils its phosphomodulatory network linked to splicing and tumorigenesis.Frontiers in bioinformatics · 2026Article
- Diverse roles of YTHDC1 in chromatin and blood cancers.Frontiers in genetics · 2026Review
- RNA modifications in cancer stem cells: molecular mechanisms and targeted therapeutic strategies.Frontiers in cell and developmental biology · 2026Review
- ALKBH5 deficiency suppresses hepatocarcinogenesis in mice via mActa pharmacologica Sinica · 2026Article
- The METTL3-YTHDC1 axis mediates architectural RNA mMolecular cancer · 2025Article
- mActa pharmaceutica Sinica. B · 2025Review
- Review
47 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 6 institutions in 2 countries.
Funding
Abstract
YTHDC1 has distinct functions as a nuclear N6-methyladenosine (m6A) reader in regulating RNA metabolism. Here we show that YTHDC1 is overexpressed in acute myeloid leukemia (AML) and that it is required for the proliferation and survival of human AML cells. Genetic deletion of Ythdc1 markedly blocks AML development and maintenance as well as self-renewal of leukemia stem cells (LSCs) in vivo in mice. We found that Ythdc1 is also required for normal hematopoiesis and hematopoietic stem and progenitor cell (HSPC) maintenance in vivo. Notably, Ythdc1 haploinsufficiency reduces self-renewal of LSCs but not HSPCs in vivo. YTHDC1 knockdown has a strong inhibitory effect on proliferation of primary AML cells. Mechanistically, YTHDC1 regulates leukemogenesis through MCM4, which is a critical regulator of DNA replication. Our study provides compelling evidence that shows an oncogenic role and a distinct mechanism of YTHDC1 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.