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Life sciences · Journal article
Theoretical and Natural Science · September 22, 2026
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Metastasis, not the primary tumor, accounts for most deaths from gastrointestinal (GI) cancers, and GI metastases display striking organ tropism: colorectal, pancreatic, and gastric cancers preferentially colonize the liver, gastric cancer the peritoneum, esophageal squamous cell carcinoma the lymph nodes. Yet the molecular logic instructing disseminating cells where to land remains poorly understood. N6-methyladenosine (m6A), the most abundant internal mRNA modification, is dynamically installed, removed, and interpreted by dedicated Writers, Erasers, and Readers. Emerging evidence positions m6A as an architect of organotropism acting at three levels. At the seed level, m6A programs metastatic competence — epithelial–mesenchymal transition, stemness, and anoikis resistance. On the route level, m6A regulates chemokine gradients (CXCL1/CXCR2) and adhesion programs involved in portal, lymphatic, and transcoelomic spread of cancer cells. On the soil level, tumor-derived exosomes containing m6A-modified RNAs or RNAs sorted by m6A readers can remotely shape the pre-metastatic niche (PMN) in liver and abdomen through myeloid-derived suppressor cell recruitment, macrophage polarization, and stromal activation before actual arrival of tumor cells. Since PMN establishment is upstream of the onset of metastasis, the therapeutic window has been established within which m6A-targeting drugs such as METTL3 inhibitors, FTO inhibitors, and siRNAs loaded on nanoparticles may be used as adjuvant antitumoral therapy. In this review, we reframe the GI m6A field with the concept of seed-route-soil, describe organ tropism signatures, and speculate on how epitranscriptome modulation could turn the problem of organotropism into its potential solution.