Journal
CANCER CELL
Volume 17, Issue 1, Pages 53-64Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2009.11.021
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Funding
- National Institutes of Health [CA89720, CA107548, CA78810, CA90917, CA118005, HL54131]
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Inhibitor-of-Apoptosis (IAP) proteins contribute to tumor progression, but the requirements of this pathway are not understood. Here, we show that intermolecular cooperation between XIAP and survivin stimulates tumor cell invasion and promotes metastasis. This pathway is independent of IAP inhibition of cell death. Instead, a survivin-XIAP complex activates NF-kappa B, which in turn leads to increased fibronectin gene expression, signaling by beta 1 integrins, and activation of cell motility kinases FAK and Src. Therefore, IAPs are direct metastasis genes, and their antagonists could provide antimetastatic therapies in patients with cancer.
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