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Shift of syndecan-1 expression from epithelial to stromal cells during progression of solid tumours

D Mennerich1, A Vogel, I Klaman

  • 1Research Laboratories of Schering AG, Enabling Technologies, Müllerstr. 178, 13342 Berlin, Germany. detlev.mennerich@schering.de

European Journal of Cancer (Oxford, England : 1990)
|June 5, 2004
PubMed

Insights

Researchers discovered a second syndecan-1 (SDC-1) mRNA isoform, finding both transcripts coexpressed in normal and tumor tissues. Upregulation of SDC-1 in tumors primarily stems from surrounding stromal cells, not cancer cells themselves.

Area of Science:

  • Molecular biology
  • Cancer research
  • Cell biology

Background:

  • Syndecan-1 (SDC-1) is crucial for cell adhesion, migration, and maintaining epithelial structure.
  • SDC-1 expression is linked to inhibited invasiveness and epithelial morphology.
  • A second SDC-1 mRNA isoform was identified, prompting further investigation into its expression patterns.

Purpose of the Study:

  • To identify and characterize a second SDC-1 mRNA isoform.
  • To investigate the expression of both SDC-1 transcripts in normal and malignant tissues.
  • To determine the cellular origin of SDC-1 upregulation in tumor tissues.

Main Methods:

  • Identification of a novel SDC-1 mRNA isoform.
  • Analysis of SDC-1 transcript expression in various tissues using Cancer-profiling array (CPA).
  • Oligonucleotide array-based expression analysis in microdissected carcinoma cells.
  • In situ hybridization and immunohistochemistry to localize SDC-1 expression.

Main Results:

  • Both SDC-1 mRNA transcripts were found to be coexpressed at equal levels in all analyzed tissues and organs.
  • Cancer-profiling array analysis revealed significant SDC-1 upregulation in tumor tissues compared to normal tissues.
  • In situ hybridization and immunohistochemistry identified stromal cells, specifically spindle cells with myofibroblastic differentiation, as the source of SDC-1 upregulation in the connective tissue surrounding specific carcinomas (breast, lung, colon, bladder).

Conclusions:

  • The study identified a second SDC-1 mRNA isoform with coexpression across tissues.
  • SDC-1 upregulation in tumors originates from reactive stromal myofibroblasts, not tumor cells.
  • These SDC-1-expressing stromal cells may play a role in tumor dedifferentiation and metastasis development.

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