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HER-2/neu-mediated down-regulation of biglycan associated with altered growth properties

Christian V Recktenwald1, Sandra Leisz, André Steven

  • 1Martin Luther University Halle-Wittenberg, Institute of Medical Immunology, 06112 Halle (Saale), Germany.

The Journal of Biological Chemistry
|May 15, 2012
PubMed

Insights

Biglycan (Bgn) expression decreases in HER-2/neu-transformed cells, reducing their growth and migration. Protein kinase C (PKC) pathway activation restores Bgn, inhibiting neoplastic properties.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Oncology

Background:

  • Biglycan (Bgn) is an extracellular matrix proteoglycan implicated in cell behavior.
  • Altered Bgn expression is observed in human tumors, but its role in cancer development is unclear.

Purpose of the Study:

  • To investigate the role of biglycan (Bgn) in oncogenic transformation mediated by the HER-2/neu oncogene.
  • To elucidate the regulatory mechanisms controlling Bgn expression in transformed cells.

Main Methods:

  • Utilized an in vitro model of oncogenic transformation using HER-2/neu-transformed murine and human cells.
  • Assessed Bgn expression, secretion, and cellular functions (growth, migration, wound closure).
  • Investigated the involvement of signaling pathways, including protein kinase C (PKC) and cAMP response element binding protein (CREB).

Main Results:

  • Down-regulation of Bgn expression and altered isoform secretion were observed in HER-2/neu-transformed cells, correlating with reduced growth and migration.
  • Silencing Bgn in normal fibroblasts enhanced their growth and migration.
  • Bgn expression in transformed cells was restored by inhibiting the PKC pathway, with CREB identified as a key regulator.

Conclusions:

  • Biglycan (Bgn) acts as an inhibitor of key properties associated with HER-2/neu-mediated neoplastic transformation.
  • The protein kinase C (PKC) signaling cascade inversely modulates Bgn expression, highlighting a novel regulatory mechanism in cancer progression.

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