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Analyzing the Communication Between Monocytes and Primary Breast Cancer Cells in an Extracellular Matrix Extract ECME-based Three-dimensional System
10:55

Analyzing the Communication Between Monocytes and Primary Breast Cancer Cells in an Extracellular Matrix Extract ECME-based Three-dimensional System

Published on: January 8, 2018

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Soluble extracellular matrix metalloproteinase inducer (EMMPRIN, EMN) regulates cancer-related cellular functions by

Nadine Knutti1, Michael Kuepper2, Karlheinz Friedrich1

  • 1Institute of Biochemistry II, Jena University Hospital, Germany.

The FEBS Journal
|August 17, 2015
PubMed

Insights

Extracellular matrix metalloproteinase inducer (EMMPRIN) interactions influence cell behavior. This study reveals how soluble EMMPRIN affects breast cancer cell proliferation and migration, uncovering a feedback loop and Wnt pathway activation.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Molecular Oncology

Background:

  • Extracellular matrix metalloproteinase inducer (EMMPRIN) is a glycoprotein involved in development and disease.
  • EMMPRIN mediates homotypic interactions, impacting various cellular functions.
  • Understanding EMMPRIN's structural basis and signaling is crucial for cancer research.

Purpose of the Study:

  • To characterize the structural basis of EMMPRIN-EMMPRIN receptor (EMNR) contacts.
  • To investigate the functional effects of soluble EMMPRIN on breast carcinoma cells.
  • To elucidate the signaling pathways triggered by EMMPRIN interactions.

Main Methods:

  • Utilized recombinant soluble EMMPRIN domain (rhsEMN) for binding and functional assays.
  • Assessed effects on MCF-7 breast carcinoma cell proliferation and migration.
  • Analyzed upregulation of EMMPRIN and MMP-14.
  • Investigated Wnt pathway activation in HEK-293 cells.

Main Results:

  • rhsEMN bound to cell surface EMMPRIN with high affinity and was internalized.
  • The N-terminal Ig domain mediates homotypic EMMPRIN contact.
  • rhsEMN stimulated MCF-7 cell proliferation but reduced migration.
  • A feedback mechanism involving EMMPRIN and MMP-14 upregulation was observed.
  • rhsEMN triggered the oncogenic Wnt pathway.

Conclusions:

  • EMMPRIN homotypic interactions are structurally defined and functionally significant.
  • Soluble EMMPRIN modulates breast cancer cell behavior, promoting proliferation and inhibiting migration.
  • EMMPRIN signaling involves a feedback loop and activation of the Wnt pathway, relevant to malignancy.
Keywords:
MMPsWnt pathwaybreast cancermembrane proteinsprotein glycosylation

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