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Vol. 11, Issue 4, 1357-1367, April 2000
and
*Lawrence Berkeley National Laboratory, Life Sciences Division,
Berkeley, California 94720; and To identify genes misregulated in the final stages of breast
carcinogenesis, we performed differential display to compare the gene
expression patterns of the human tumorigenic mammary epithelial cells,
HMT-3522-T4-2, with those of their immediate premalignant progenitors,
HMT-3522-S2. We identified a novel gene, called anti-zuai-1 (AZU-1),
that was abundantly expressed in non- and premalignant cells and
tissues but was appreciably reduced in breast tumor cell types and in
primary tumors. The AZU-1 gene encodes an acidic 571-amino-acid protein
containing at least two structurally distinct domains with potential
protein-binding functions: an N-terminal serine and proline-rich domain
with a predicted immunoglobulin-like fold and a C-terminal coiled-coil
domain. In HMT-3522 cells, the bulk of AZU-1 protein resided in a
detergent-extractable cytoplasmic pool and was present at much lower
levels in tumorigenic T4-2 cells than in their nonmalignant
counterparts. Reversion of the tumorigenic phenotype of T4-2 cells, by
means described previously, was accompanied by the up-regulation
of AZU-1. In addition, reexpression of AZU-1 in T4-2 cells, using viral
vectors, was sufficient to reduce their malignant phenotype
substantially, both in culture and in vivo. These results indicate that
AZU-1 is a candidate breast tumor suppressor that may exert its effects by promoting correct tissue morphogenesis.
Structural Cell Biology
Unit, Institute of Medical Anatomy, The Panum Institute, DK-2100
Copenhagen, Denmark
Present address: Incyte Pharmaceuticals,
3160 Porter Drive, Palo Alto, CA 94304.
§
Corresponding author. E-mail address:
MJBissell{at}lbl.gov.
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