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[Cancer Research 65, 2761-2769, April 1, 2005]
© 2005 American Association for Cancer Research

Cell and Tumor Biology

Hypoxia Stimulates Carcinoma Invasion by Stabilizing Microtubules and Promoting the Rab11 Trafficking of the {alpha}6ß4 Integrin

Sang-Oh Yoon, Sejeong Shin and Arthur M. Mercurio

Division of Cancer Biology and Angiogenesis, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts

Requests for reprints: Arthur M. Mercurio, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Research North, Boston, MA 02215. Phone: 617-667-7714; Fax: 617-667-5531; E-mail: amercuri{at}bidmc.harvard.edu.

Hypoxia plays a key role in tumor cell survival, invasion, and metastasis. Here we show that hypoxia increases tumor cell invasion by the modulation of Rab11, an important molecule for vesicular trafficking, especially membrane protein recycling and translocation of proteins from trans-Golgi network to plasma membrane. Dominant-negative Rab11 dramatically decreased hypoxia-induced invasion of MDA-MB-231 breast carcinoma cells without affecting cell apoptosis. Hypoxia-induced Rab11 trafficking is regulated by microtubule stability, as evidenced by the findings that hypoxia increases Glu tubulin and that colchicine blocks Rab11 trafficking and invasion. Inhibition of GSK-3ß activity by hypoxia seems to be central to microtubule stabilization and invasion. In fact, expression of a dominant-negative GSK-3ß was sufficient to stimulate invasion in normoxia. One target of Rab11-mediated trafficking that contributes to invasion is the integrin {alpha}6ß4. Hypoxia induced a significant increase in {alpha}6ß4 surface expression but it had no effect on the surface expression of {alpha}3ß1. This increase is dependent on Rab11 and stable microtubules. In summary, we identify vesicle trafficking as a novel target of hypoxic stimulation that is important for tumor invasion.

Key Words: hypoxia • invasion • Rab11 • microtubules • integrin




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