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J. Biol. Chem., Vol. 276, Issue 18, 15547-15553, May 4, 2001
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From the CEACAM1 is a cell-cell adhesion molecule that
mediates homophilic cell adhesion. In addition, CEACAM1 was also shown
to suppress the growth of prostate, breast, and colon tumors.
Structural and functional analyses showed that the adhesion activity of
CEACAM1 is mediated by its extracellular domain while its cytoplasmic domain is necessary and sufficient for growth-inhibitory activity. The
signal pathways leading to CEACAM1-mediated growth suppression are not
known. We studied the importance of phosphorylation of serine 503 in
this growth-inhibitory signaling pathway. Full-length CEACAM1 was found
to be phosphorylated in vivo in both tyrosine and serine
residues. Mutation of tyrosine 488 to phenylalanine did not abolish the
tumor-suppressive activity of CEACAM1, suggesting that phosphorylation
at tyrosine 488 is not critical for CEACAM1's tumor-suppressive
activity. Although expression of CEACAM1's cytoplasmic domain
inhibited the growth of DU145 prostate cancer cells in vivo, mutation of serine 503 to alanine abolished the
growth-inhibitory activity. In addition, the change of serine 503 to
aspartic acid produced tumor-suppressive activity similar to that of
the wild-type CEACAM1. These results suggested that phosphorylation at
serine 503 is essential for CEACAM1's growth-inhibitory function
in vivo.
Signal Transduction by the CEACAM1 Tumor Suppressor
PHOSPHORYLATION OF SERINE 503 IS REQUIRED FOR GROWTH-INHIBITORY
ACTIVITY*
,,
Department of Molecular Pathology, The
University of Texas M. D. Anderson Cancer Center, Houston, Texas
77030, the § Department of Pediatrics and Center for
Academic and Reading Skills, The University of Texas-Houston Health
Science Center, Houston, Texas 77030, and the ¶ Department of
Medical Oncology, Rhode Island Hospital, Brown University, Providence,
Rhode Island 02906
*
This work was supported by Grant CA64856 (to S. H. L.),
Core Grant CA16672 (to M. D. Anderson Cancer Center), and
Predoctoral Training Grant T32 CA67759 (to V. T. E.) from the
National Institutes of Health.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of Molecular
Pathology, Box 89, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Blvd., Houston, TX 77030. Tel.: 713-794-1559; Fax: 713-794-4672; E-mail: slin@notes.mdacc.tmc.edu.
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