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Is Down-Regulated in Human Breast Cancer Cells1
Equipe Facteurs de Croissance, Laboratoire de Biologie du Développement, UPRES-EA 1033, Villeneuve d’Ascq, France [A-S. V-E., X. L. B., B. B., H. H.]; Laboratoire de Chimie Biologique, UMR 8576 Centre National de la Recherche Scientifique, Université des Sciences et Technologies de Lille, 59650 Villeneuve d’Ascq Cedex, France [J. L.]; Laboratoire d’Oncologie Moléculaire Humaine, Centre de Lutte Contre le Cancer, de la région Nord-Pas de Calais (Centre Oscar Lambret), BP307, 59020 Lille, France [H. L., F. R., J-P. P.]; and Department of Anatomical Sciences, University of Queensland, St. Lucia, Queensland 4072, Australia [V. N.]
The class of molecular chaperones known as 14-3-3 is involved in the
control of cellular growth by virtue of its apparent regulation of
various signaling pathways, including the Raf/mitogen-activated protein
kinase pathway. In breast cancer cells, the 
form of 14-3-3 has been
shown to interact with cyclin-dependent kinases and to control
the rate of entry into mitosis. To test for a direct role for 14-3-3 in
breast epithelial cell neoplasia, we have quantitated 14-3-3 protein
levels using a proteomic approach based on two-dimensional
electrophoresis and matrix-assisted laser desorption/ionization mass
spectrometry (MALDI-TOF). We show here that 14-3-3 protein is
strongly down-regulated in the prototypic breast cancer cell lines
MCF-7 and MDA-MB-231 and in primary breast carcinomas as compared with
normal breast epithelial cells. In contrast, levels of the 
, ß,
, or 
isoforms of 14-3-3 were the same in both normal and
transformed cells. The data support the idea that 14-3-3 is involved
in the neoplastic transition of breast epithelial cells by virtue of
its role as a tumor suppressor; as such, it may constitute a robust
marker with clinical efficacy for this pathology.
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