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Related Experiment Videos

Memo mediates ErbB2-driven cell motility.

Romina Marone1, Daniel Hess, David Dankort

  • 1Friedrich Miescher Institute for Biomedical Research, Maulbeerstrasse 66, CH-4058 Basel, Switzerland.

Nature Cell Biology
|May 25, 2004
PubMed
Summary
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A novel molecule, Memo, is crucial for ErbB2-driven breast cancer cell motility. Memo relays signals to the cytoskeleton, impacting metastasis and poor outcomes in ErbB2-positive cancers.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Increased ErbB2 expression in cancer correlates with aggressive, metastatic disease and poor prognosis.
  • The molecular mechanisms driving ErbB2-dependent cell motility and metastasis remain largely unknown.

Purpose of the Study:

  • To elucidate the molecular basis of ErbB2-driven cell motility and metastasis.
  • To identify novel mediators involved in ErbB2 signaling pathways controlling cell migration.

Main Methods:

  • Investigated the role of signaling molecules (MAPK, PI(3)K, Src) in Neu/ErbB2-dependent cell functions.
  • Analyzed the impact of specific Neu/ErbB2 phosphorylation sites (Tyr 1201, Tyr 1227) on cell migration.
  • Identified and characterized a novel protein, Memo, interacting with phosphorylated ErbB2.

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Main Results:

  • Activation of MAPK, PI(3)K, and Src is essential for Neu/ErbB2-driven lamellipodia formation and breast carcinoma cell motility.
  • Efficient cell migration requires Neu/ErbB2 phosphorylation at Tyr 1201 or Tyr 1227.
  • Memo interacts with phospho-Tyr 1227, likely via the Shc adaptor protein.
  • Memo-defective cells exhibit defects in microtubule extension towards the cell cortex, despite lamellipodia formation.

Conclusions:

  • Memo is a key mediator of ErbB2-driven cell motility, controlling the relay of chemotactic signals to the microtubule cytoskeleton.
  • Understanding Memo's role provides insights into ErbB2-mediated metastasis and potential therapeutic targets for aggressive breast cancers.