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Merck
  • ArgBP2-dependent signaling regulates pancreatic cell migration, adhesion, and tumorigenicity.

ArgBP2-dependent signaling regulates pancreatic cell migration, adhesion, and tumorigenicity.

Cancer research (2008-06-19)
David Taieb, Julie Roignot, Frédéric André, Stéphane Garcia, Bénédicte Masson, Anne Pierres, Juan-Lucio Iovanna, Philippe Soubeyran
摘要

The poor prognosis of pancreatic cancer is due to rapid locoregional invasion, the early development of metastases, and the limited efficacy of current therapies. To date, none of the identified oncogenes and suppressors involved in this disease have led to efficient treatments. Here, we describe that the scaffold protein ArgBP2 is repressed during oncogenic transformation of the pancreas. We could show, using a pancreatic cancer cell line model, that this repression of ArgBP2 participates in the progression of this disease. Interestingly, in vitro analyses revealed that the antitumoral potential of ArgBP2 is linked to the control of cell adhesion and migration rather than to the regulation of cell proliferation or sensitivity to apoptosis. Moreover, we could detail part of the molecular mechanism responsible by identifying new ArgBP2-interacting proteins, and show that this function is partly achieved by the control of a WAVE/PTP-PEST/c-Abl signaling complex. These findings point to a new mechanism of pancreatic cancer progression leading to invasion and metastasis and suggest that the ArgBP2 signaling pathway could represent a new target for cancer therapy.

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Sigma-Aldrich
单克隆抗-FLAG® M2 小鼠抗, clone M2, purified immunoglobulin (Purified IgG1 subclass), buffered aqueous solution (10 mM sodium phosphate, 150 mM NaCl, pH 7.4, containing 0.02% sodium azide)
Sigma-Aldrich
Monoclonal Anti-Protein Tyrosine Phosphatase PEST antibody produced in mouse, clone AG25, purified immunoglobulin