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June 26, 2026Science AdvancesOpen Access

METTL3 regulates exocytosis independently of m 6 A

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Authors

MEMargalida Esteva-SociasDBDevi Prasad BhattaraiCACyrinne Achour

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Overview

Preclinical study demonstrates that cytoplasmic METTL3 drives exocytosis and invasion in breast cancer models, indicating an enzymatic-independent role in tumor progression.

Key Points

  • To determine the catalytic-independent mechanisms through which METTL3 regulates exocytosis, vesicle trafficking, and invasion in breast cancer.
  • Examined subcellular localization of METTL3 in patient-derived breast cancer tumor specimens.
  • Characterized molecular interactions between cytoplasmic METTL3 and EXOC7, as well as EXOC7 alternative splicing.
  • Compared METTL3 genetic depletion against catalytic inhibition in vitro to evaluate effects on vesicle trafficking, secretome composition, invadopodia formation, and collagen matrix invasion.
  • METTL3 mislocalizes to the cytoplasm in patient breast cancer tumors, where it directly interacts with and stabilizes the exocytosis regulator EXOC7 while also modulating its alternative splicing.
  • METTL3 knockdown impairs vesicle trafficking, disrupts the cancer secretome, suppresses invadopodia assembly, and halts collagen matrix invasion.
  • Selective pharmacological inhibition of METTL3 catalytic activity does not alter invadopodia formation or matrix invasion, confirming these phenotypes operate via non-catalytic mechanisms.

Cite This Study

Esteva-Socias et al. (2026) studied this question.

synapsesocial.com/papers/6a91b8da31a390edffa391cdhttps://doi.org/10.1126/sciadv.adz2434
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Also Consider

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  1. 1Unraveling the independent role of METTL3 in m6A modification and tumor progression in esophageal squamous cell carcinoma2024 · 11 citations
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  5. 5METTL3-mediated activation of Sonic Hedgehog signaling promotes breast cancer progression2025