ArticleThe Journal of biological chemistry2026
Syndecan-2 enhances invasive motility in colon cancer cells via a laminin-332-integrin α6β1 axis.
Article in The Journal of biological chemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Syndecan-2 (SDC-2) is a key regulator of colon cancer progression, but its cooperation with integrins in cell motility is not fully understood. Here, we show that SDC-2 overexpression in HT29 colon cancer cells (HT29-S2W) enhances adhesion, spreading, and migration on laminin-332, an extracellular matrix component linked to poor prognosis. These effects correlate with increased basal membrane localization of integrin α6, as well as elevated expression and deposition of laminin-332 subunits (α3, β3, and γ2), thereby promoting laminin-332 assembly within the extracellular matrix. Proximity ligation assays revealed enhanced interactions between SDC-2 and integrin α6β1 following SDC-2 overexpression, indicating coordinated signaling mediated by laminin-332. Notably, HT29-S2W cells adhered more efficiently to full-length laminin-332 containing the SDC-2-binding LG4/5 modules of the laminin α3 chain than to truncated laminin-332 lacking these modules. Furthermore, both an anti-integrin α6 antibody and a laminin-α3-derived peptide (A3G75aR) significantly inhibited adhesion to full-length laminin-332. In metastatic DLD-1 cells, which express high levels of SDC-2 and laminin-332, combined treatment with the antibody and peptide markedly suppressed cell migration and invasion. Collectively, these findings identify an SDC-2-laminin-332-integrin α6β1 axis that drives invasive motility and may represent a promising therapeutic target in metastatic colorectal cancer.
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