METTL3
Overview
METTL3 encodes methyltransferase-like 3, the catalytic subunit of the m6A (N6-methyladenosine) RNA methyltransferase complex. As the primary writer of the most abundant internal mRNA modification in eukaryotes, METTL3 regulates mRNA stability, translation, and splicing. It is upregulated in multiple cancer types and plays oncogenic roles by stabilizing transcripts encoding proliferative and survival factors.
Alterations observed in the corpus
- METTL3 is an LPS-inducible m6A methyltransferase that promotes cholangiocarcinoma cell migration and invasion via the PI3K/AKT pathway; LPS/TLR4-driven METTL3 activation links gut dysbiosis to CCA progression (Ke J 2024, cited in review). PMID:25608663
Cancer types (linked)
- CHOL / IHCH: METTL3 upregulated by LPS stimulation; drives CCA migration and invasion through PI3K/AKT signaling, providing a mechanistic link between gut microbiota dysbiosis (elevated portal LPS) and tumor invasiveness. PMID:25608663
Co-occurrence and mutual exclusivity
- Operates downstream of LPS/TLR4 signaling in the gut-liver axis context; pathway convergence with IL-6/STAT3 inflammatory cascade. PMID:25608663
Therapeutic relevance
- METTL3 inhibition represents a potential therapeutic angle for disrupting the LPS-driven oncogenic cascade in cholangiocarcinoma, though no clinical agents are reported in this corpus. PMID:25608663
Open questions
- Whether METTL3 overexpression in CCA is driven primarily by LPS/TLR4 signaling versus other oncogenic inputs, and whether specific m6A targets mediate the pro-invasive phenotype, requires direct experimental validation. PMID:25608663
Sources
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