ArticleJournal of hematology & oncology2024
METTL16 promotes liver cancer stem cell self-renewal via controlling ribosome biogenesis and mRNA translation.
Article in Journal of hematology & oncology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 72 citations in OpenAlex.
- TRIM32-mediated ubiquitination of STING promotes glycolysis and tumor progression.Cell death and differentiation · 2026Article
- Metabolic licensing of quiescent glioblastoma activation and immune evasion via astrocyte-mitochondria shuttle.Nature communications · 2026Article
- Regulatory Role of Ribosome Biogenesis-Related Genes in Hepatocellular Carcinoma Prognosis and Construction of a Risk Prediction Model.Digestive diseases and sciences · 2026Article
- METTL16-mediated upregulation of LINC00665 inhibits the apoptosis of breast cancer via regulating miR-28-5p/GLG1 axis.Translational cancer research · 2026Article
- IGF2BP3 promotes glycolysis of osteosarcoma stem cells by reading RNA m⁶A to stabilize ENO1 and promote malignant biological behavior of osteosarcoma.Cell biology and toxicology · 2026Article
- Cuproptosis: potential new direction in liver-related diseases research and treatment.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- The Role of NMedComm · 2026Review
- SLC25A5 Suppresses Colorectal Cancer Growth and Metastasis Through Regulation of the EIF3A/PI3K/AKT Axis.International journal of molecular sciences · 2026Article
- METTL16 Promotes Head and Neck Squamous Cell Carcinoma Progression via m6A-Mediated Stabilization of SREBP2 mRNA and Enhanced Cholesterol Biosynthesis.Cancer medicine · 2026Article
- MOncogene · 2026Article
- Endothelial USP2a-METTL16 loop potentiates IL-6 signaling via mCell death and differentiation · 2026Article
- Filgotinib inhibits METTL3-mediated mNPJ precision oncology · 2026Article
- Article
- METTL16-mediated m6A modification of LYRM2 drives breast cancer progression by inducing CD8Journal of bioenergetics and biomembranes · 2026Article
- METTL16-mediated mJournal of experimental & clinical cancer research : CR · 2026Article
- METTL16 in cancer: Roles and regulatory mechanisms.Genes & diseases · 2026Review
- METTL13 mediated SAA1 translation maintains cancer stem cell behavior and promotes esophageal carcinoma progression.Journal of translational medicine · 2026Article
- Epitranscriptomic control of cancer hallmarks: Functions, mechanisms, and therapeutics of RNA modifications.Cancer cell · 2026Review
- Single-cell multi-omics reveals DUSP9 as a key regulator of cancer stemness and a potential therapeutic target in hepatocellular carcinoma.Journal of translational medicine · 2026Article
- Emerging roles of tRNA modification-mediated codon-specific translational reprogramming in cancer biology.Cell death & disease · 2026Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
35 authors at 7 institutions in 2 countries.
Funding
Abstract
backgroundWhile liver cancer stem cells (CSCs) play a crucial role in hepatocellular carcinoma (HCC) initiation, progression, recurrence, and treatment resistance, the mechanism underlying liver CSC self-renewal remains elusive. We aim to characterize the role of Methyltransferase 16 (METTL16), a recently identified RNA N
methodsLiver-specific Mettl16 conditional KO (cKO) mice were generated to assess its role in HCC pathogenesis and normal hepatogenesis. Hydrodynamic tail-vein injection (HDTVi)-induced de novo hepatocarcinogenesis and xenograft models were utilized to determine the role of METTL16 in HCC initiation and progression. A limiting dilution assay was utilized to evaluate CSC frequency. Functionally essential targets were revealed via integrative analysis of multi-omics data, including RNA-seq, RNA immunoprecipitation (RIP)-seq, and ribosome profiling.
resultsMETTL16 is highly expressed in liver CSCs and its depletion dramatically decreased CSC frequency in vitro and in vivo. Mettl16 KO significantly attenuated HCC initiation and progression, yet only slightly influenced normal hepatogenesis. Mechanistic studies, including high-throughput sequencing, unveiled METTL16 as a key regulator of ribosomal RNA (rRNA) maturation and mRNA translation and identified eukaryotic translation initiation factor 3 subunit a (eIF3a) transcript as a bona-fide target of METTL16 in HCC. In addition, the functionally essential regions of METTL16 were revealed by CRISPR gene tiling scan, which will pave the way for the development of potential inhibitor(s).
conclusionsOur findings highlight the crucial oncogenic role of METTL16 in promoting HCC pathogenesis and enhancing liver CSC self-renewal through augmenting mRNA translation efficiency.
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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.