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A more recent version of this article appeared on December 1, 2006
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Submitted on November 22, 2005
Revised on August 31, 2006
Accepted on September 7, 2006
*Inserm U752, Collège de France, 75005 Paris, France; Department of Pathology-Neurooncology, Hopital Sainte-Anne, 75674 Paris Cedex 14, France; Inserm U691, Collège de France, 75005 Paris, France; Inserm U421, Faculté de Médecine, 94010 Creteil, France; ||Inserm U542, Hopital Paul Brousse, 94807 Villejuif Cedex, France; ¶Cancer Research Center of Hawaii, University of Hawaii at Manoa, Honolulu, HI 96813
Monitoring Editor: Anne Ridley
PEA-15, a phosphoprotein enriched in astrocytes, inhibits both apoptosis and proliferation in normal and cancerous cells. Here, analysis of PEA-15 expression in glioblastoma organotypic cultures revealed low levels of PEA-15 in tumor cells migrating away from the explants, regardless of the expression levels in the originating explants. Because glioblastomas are highly invasive primary brain tumors that can originate from astrocytes, we explored the involvement of PEA-15 in the control of astrocyte migration. PEA-15-/- astrocytes presented an enhanced motility in vitro as compared with their wild-type counterparts. Accordingly, NIH-3T3 cells transfected by GFP-PEA-15 displayed a reduced migration. Reexpression of PEA-15 restored PEA-15-/- astrocyte motility to wild-type levels. Pharmacological manipulations excluded a participation of ERK/MAPK, PI3K/Akt and CaMKII in this effect of PEA-15. In contrast, treatment by bisindolylmaleimide, Gö6976 and rottlerin, and chronic application of PMA and/or bryostatin-1 indicated that PKC
mediated PEA-15 inhibition of astrocyte migration. PEA-15-/- astrocytes constitutively expressed a 40-kDa form of PKC that was down-regulated upon PEA-15 reexpression. Taken together these data reveal a new function for PEA-15 in the inhibitory control of astrocyte motility through a PKC-dependent pathway involving the constitutive expression of a catalytic fragment of PKC.
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