ArticleCell death & disease2025
HOTAIR requires epitranscriptomic modification to exert its pivotal epigenetic role in Epithelial to Mesenchymal Transition.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Chromatin remodelling: a driving force in reverse mechanotransduction.RNA biology · 2026Review
- The crosstalk between RNA m6A modification and protein lactylation: emerging insights into tumor progression.Oncogene · 2026Review
- The lncRNA-m6A axis in cancer: a bidirectional regulatory network in tumor progression and therapeutic resistance.Journal of translational medicine · 2026Review
- The "Hit-and-Run" legacy: epigenetic locking and the survival switch in H. pylori-associated gastric cancer.Cell death discovery · 2026Review
- Interplay between the RBP SYNCRIP and RNA methylation in determining sEV miRNA-cargo and function in cell-to-cell communication.Cell death & disease · 2026Article
- Conserved structural features of the lncRNA HOTAIR in breast cancer cells.bioRxiv : the preprint server for biology · 2026Article
- Extracellular vesicles from activated Vδ2 T cells inhibit viral replication and enhance adaptive antiviral immunity.Journal of translational medicine · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
While m6A epitranscriptomic modification has been shown to impact several mRNAs maturation, stability/degradation, nuclear/cytoplasm export and translation regulation, its impact on lncRNAs activity is yet largely uncharacterized. Here, we show that the silencing of the m6A writer METTL3 inhibits Epithelial to Mesenchymal Transition (EMT), morphological, migratory and invasive features of TGFβ-treated epithelial cells as well as of tumor cells. Building on previous evidence pinpointing the lncHOTAIR as a mandatory element for epithelial genes' repression triggering EMT, here we uncover a dominant role of an epitranscriptomic modification on the epigenetic function of this lncRNA. Mechanistically, HOTAIR is m6A-modified on the interaction domains with both the master transcriptional factor of EMT SNAIL and the general chromatin modifier EZH2. This epitranscriptomic modification is necessary for the interaction between HOTAIR and SNAIL/EZH2 and in turn for HOTAIR-dependent epigenetic repression on SNAIL-targeted epithelial genes. Impairing m6A modification impedes the assembling of the tripartite SNAIL/HOTAIR/EZH2 complex and in turn blocks EMT accomplishment. Overall, we unveil that the epitranscriptomic modification m6A has a dominant role on the epigenetic function of a lncRNA.
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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 Socratic graph.