[Expression of early placenta insulin-like growth factor (EPIL) in breast cancer cells provides an autocrine loop with enhancement of predominantly HER-2-related invasivity]

Verh Dtsch Ges Pathol. 2005:89:201-6.
[Article in German]

Abstract

Aims: Recently, we were able to show that the expression of early placenta insulin like growth factor (EPIL) is expressed by highly motile HER-2-positive breast cancer cells in vitro (Brandt et al., Cancer Res. 2002) in Paget cells in vivo and indicates a poor clinical prognosis, irrespectively of other prognostic factors.

Methods: In order to demonstrate the interplay between HER-2 and Epil we established a cellular model for high simultaneous Epil and HER-2 expression. The HER-2-positive breast cancer cell line SKBR3 was modified with an EPIL expression vector. In addition, an assay for the knockdown of EPIL-expression via siRNA was established. Erk1/2 expression was measured via Western Blot. The phenotype of the viable cells was determined by laser scan microscopy.

Results: Epil overexpression in SKBR3 cells resulted in fast and frequent protrusion formation of the cells shown by laser scan microscopy. The cells were further characterized by a significantly increased invasiveness, which could be reversed by Epil specific siRNA treatment. Increased invasiveness and morphological changes were associated with a decreased erk1/2 phosphorylation.

Conclusions: These data further supports the assumption that EPIL might provide an autocrine loop in HER-2-positive breast cancer cells that enforce metastasis, conceivably escape from adjuvant therapy and in consequence poor clinical outcome. A tight interaction between HER-2 and EPIL in invasive breast cancer cells is therefore likely. The exact mechanims remain to be elucidated.

Publication types

  • English Abstract

MeSH terms

  • Breast Neoplasms / genetics*
  • Breast Neoplasms / pathology*
  • Female
  • Gene Expression Regulation, Neoplastic
  • Genes, erbB-2
  • Humans
  • Immunohistochemistry
  • Intercellular Signaling Peptides and Proteins / genetics*
  • Neoplasm Invasiveness
  • Plasmids
  • RNA, Neoplasm / genetics
  • RNA, Neoplasm / isolation & purification
  • RNA, Small Interfering / genetics
  • Receptor, ErbB-2 / genetics*
  • Transfection

Substances

  • INSL4 protein, human
  • Intercellular Signaling Peptides and Proteins
  • RNA, Neoplasm
  • RNA, Small Interfering
  • Receptor, ErbB-2