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Syndesmos functions as a tumor suppressor by facilitating epithelial cell adhesion mediated by interactions of

Jisun Hwang1, Ga-Eun Lim2, Bohee Jang1

  • 1Department of Life Sciences, Ewha Womans University, Seoul, South Korea.

Cell Death & Disease
|May 19, 2026
PubMed

Insights

Syndesmos (SDOS) suppresses colon cancer by promoting epithelial structure and cell adhesion. Lower SDOS levels correlate with increased metastasis and poorer patient survival, highlighting its tumor-suppressive role.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Syndesmos (SDOS) regulates cytoskeletal organization and interacts with syndecan-4.
  • SDOS is under-expressed in highly metastatic colon cancer cells (HCT116) compared to weakly metastatic cells (HT29).

Purpose of the Study:

  • To investigate the role of SDOS in colon cancer development and metastasis.
  • To elucidate the molecular mechanisms by which SDOS affects cancer cell behavior and adhesion.

Main Methods:

  • Overexpression and siRNA-mediated knockdown of SDOS in colon cancer cell lines (HCT116, HT29, CT26-luc).
  • Assessment of cell migration, proliferation, morphology, and expression of epithelial markers.
  • Analysis of cell-cell and cell-extracellular matrix (ECM) junction formation, including E-cadherin, syndecan-4, and β-catenin interactions.
  • Evaluation of SDOS expression in human colon cancer tissues and correlation with patient survival.
  • In vivo studies using HCT116 xenograft and CT26-luc orthotopic mouse models.

Main Results:

  • SDOS overexpression reduced migration and proliferation in HCT116 cells, while SDOS knockdown increased these activities in HT29 cells.
  • SDOS promoted epithelial morphology, enhanced cell-cell/cell-ECM junctions, and increased expression of epithelial markers like E-cadherin.
  • SDOS directly interacted with E-cadherin and β-catenin, strengthening adherens junctions.
  • Reduced SDOS expression was observed in colon cancer tissues and associated with poor patient survival.
  • In vivo, SDOS overexpression inhibited tumor growth, whereas SDOS silencing accelerated tumor growth and metastasis.

Conclusions:

  • SDOS acts as a tumor suppressor in colon cancer, inhibiting development and metastasis.
  • SDOS maintains epithelial architecture and promotes cell adhesion through interactions with E-cadherin and β-catenin.
  • SDOS is a potential therapeutic target for improving colon cancer prognosis.

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