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<p>Syndesmos (SDOS), which regulates cytoskeletal organization via interaction with syndecan-4 in fibroblasts, was under-expressed in highly metastatic HCT116 colon cancer cells compared to weakly metastatic HT29 cells. SDOS overexpression decreased migration and proliferation of HCT116 cells, while siRNA-mediated knockdown of SDOS increased these activities in HT29 cells. SDOS overexpression in HCT116 cells promoted epithelial cell-like morphology, enhanced cell-cell and cell-ECM junction formation, and increased expression of epithelial markers. SDOS also elevated adhesion receptors, such as E-cadherin and syndecan-4, and their intracellular anchoring proteins. Notably, SDOS specifically interacted with E-cadherin and β-catenin, enhancing their interaction at cell-cell junctions in both HCT-SDOS and HT29 cells, suggesting a direct role of SDOS in adherens junction formation. In colon cancer tissue samples, SDOS expression was lower compared to adjacent normal tissues and lower SDOS levels were associated with poor post-progression survival in patients. In vivo, SDOS overexpression inhibited tumor growth in a HCT116 xenograft mouse model. Silencing SDOS in CT26-luc cells via siRNA increased tumor growth in the cecum and liver metastasis in an orthotopic model. These findings suggest that SDOS plays a critical role in suppressing colon cancer development and metastasis by maintaining epithelial architecture and promoting cell-cell and cell-ECM adhesion.</p>

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Syndesmos functions as a tumor suppressor by facilitating epithelial cell adhesion mediated by interactions of E-cadherin and β-catenin

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月19日

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  • Jisun Hwang,
  • Ga-Eun Lim,
  • Bohee Jang,
  • Jee Young Sung,
  • Hyewon Shim,
  • Hyeryun Kwon,
  • Eun Kyung Hong,
  • Eek-hoon Jho,
  • Yong-Nyun Kim,
  • Eok-Soo Oh

摘要

Syndesmos (SDOS), which regulates cytoskeletal organization via interaction with syndecan-4 in fibroblasts, was under-expressed in highly metastatic HCT116 colon cancer cells compared to weakly metastatic HT29 cells. SDOS overexpression decreased migration and proliferation of HCT116 cells, while siRNA-mediated knockdown of SDOS increased these activities in HT29 cells. SDOS overexpression in HCT116 cells promoted epithelial cell-like morphology, enhanced cell-cell and cell-ECM junction formation, and increased expression of epithelial markers. SDOS also elevated adhesion receptors, such as E-cadherin and syndecan-4, and their intracellular anchoring proteins. Notably, SDOS specifically interacted with E-cadherin and β-catenin, enhancing their interaction at cell-cell junctions in both HCT-SDOS and HT29 cells, suggesting a direct role of SDOS in adherens junction formation. In colon cancer tissue samples, SDOS expression was lower compared to adjacent normal tissues and lower SDOS levels were associated with poor post-progression survival in patients. In vivo, SDOS overexpression inhibited tumor growth in a HCT116 xenograft mouse model. Silencing SDOS in CT26-luc cells via siRNA increased tumor growth in the cecum and liver metastasis in an orthotopic model. These findings suggest that SDOS plays a critical role in suppressing colon cancer development and metastasis by maintaining epithelial architecture and promoting cell-cell and cell-ECM adhesion.