Journal
EUROPEAN JOURNAL OF CELL BIOLOGY
Volume 90, Issue 2-3, Pages 128-135Publisher
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.ejcb.2010.09.004
Keywords
Invadopodia; Acetylation; Histone deacetylase; HDAC6; Tumor cell invasion
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Funding
- Ligue Nationale contre le Cancer
- Agence Nationale pour la Recherche [ANR-08-BLAN-0111]
- Institut Curie
- CNRS
- Agence Nationale de la Recherche (ANR) [ANR-08-BLAN-0111] Funding Source: Agence Nationale de la Recherche (ANR)
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Invasion across tissue boundaries by metastatic tumor cells depends on the proteolytic degradation of the extracellular matrix, initiated by the formation of invadopodia, actin-driven membrane protrusions with matrix-degradative activity. Yet, mechanisms underlying invadopodia formation remain largely unknown. In this report, we examined the role of the histone deacetylase HDAC6 in invadopodia formation and invasion by breast cancer cells. Using small interfering RNA silencing of protein expression in highly invasive MDA-MB-231 breast adenocarcinoma cells, we show that HDAC6 is required for two-dimensional matrix proteolysis. In addition, we demonstrate that HDAC6 acts as a tubulin and cortactin deacetylase. We also report that the inhibition of HDAC6 by siRNA or treatment with HDAC inhibitor TSA results in a decreased invasion capacity of a three-dimensional type I collagen matrix by MDA-MB-231 cells. These data identify HDAC6 as a critical component of the invasive apparatus of tumor cells, in both two- and three-dimensional matrices. (C) 2010 Elsevier GmbH. All rights reserved.
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