ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2023
Silencing of IRF8 Mediated by m6A Modification Promotes the Progression of T-Cell Acute Lymphoblastic Leukemia.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 21 citations in OpenAlex.
- METTL7A-Dependent mMedComm · 2026Article
- A novel method for the identification and quantification of N6-methyladenosine motifs in RNA transcripts.Molecular biology reports · 2026Article
- CD7-Specific Polymersomal Vincristine Delivery Potentiates Chemotherapy in T‑Cell Acute Lymphoblastic Leukemia.Polymer science & technology (Washington, D.C.) · 2026Article
- Deconjugating taurocholic acid with Bifidobacterium to mitigate obesity-driven cancer progression by restoring CD8NPJ biofilms and microbiomes · 2025Article
- METTL3 Promotes Cutaneous T-Cell Lymphoma Progression by Regulating ARHGEF12 Expression.International journal of molecular sciences · 2025Article
- Modulation of the tumor immune microenvironment by Interferon Regulatory Factor 8 enhances immunotherapy in lung adenocarcinoma.Scientific reports · 2025Article
- m6A RNA methylation: a pivotal regulator of tumor immunity and a promising target for cancer immunotherapy.Journal of translational medicine · 2025Review
- METTL3 Mediated MALAT1 m6A Modification Promotes Proliferation and Metastasis in Osteosarcoma Cells.Molecular biotechnology · 2024Article
- The role and mechanism of NAT10-mediated ac4C modification in tumor development and progression.MedComm · 2024Review
- The multiple roles of interferon regulatory factor family in health and disease.Signal transduction and targeted therapy · 2024Review
- NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The roles of IRF8 in nonspecific orbital inflammation: an integrated analysis by bioinformatics and machine learning.Journal of ophthalmic inflammation and infection · 2024Article
- METTL14 promotes neuroblastoma formation by inhibiting YWHAH via an m6A-YTHDF1-dependent mechanism.Cell death discovery · 2024Article
- m5C methylation modification may be an accomplice in colorectal cancer escaping from anti-tumor effects of innate immunity-type I/III interferon.Frontiers in immunology · 2024Review
- Silencing of IRF8 Mediated by m6A Modification Promotes the Progression of T-Cell Acute Lymphoblastic Leukemia.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
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Authors and funding
15 authors at 2 institutions in 1 country.
Funding
Abstract
T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive hematological malignancy with a poor prognosis, urging for novel therapeutic targets and treatment strategies. N6-methyladenosine (m6A) is a crucial methylation modification that affects the pathogenesis of leukemia by regulating the mRNA of key genes. Interferon regulatory factor 8 (IRF8) is a crucial transcription factor for hematological lineage commitment, but its role in T-ALL is unclear. Here, IRF8 is shown to suppress T-ALL. The expression of IRF8 is abnormally silenced in patients with T-ALL. Knockout of Irf8 significantly hastens the progression of Notch1-induced T-ALL in vivo. Overexpression of IRF8 suppresses the proliferation and invasion of T-ALL cells by inhibiting the phosphatidylinositol 3-kinase/AKT signaling pathway. The fat mass- and obesity-associated protein (FTO), an m6A demethylase, is responsible for directly binding to m6A sites in 3' untranslated region of IRF8 messenger RNA (mRNA) and inducing mRNA degradation via m6A modification. Targeting the FTO-IRF8 axis is used as a proof of concept therapy; inhibition of FTO's demethylase activity drastically alleviates the proliferation of leukemic cells and prolongs the survival of T-ALL mice by restoring IRF8 expression. This study elucidates the pathogenesis of T-ALL from the perspective of epitranscriptomics and provides new insight into the genetic mechanisms and targeted therapy of T-ALL.
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