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J. Biol. Chem., Vol. 277, Issue 28, 25313-25322, July 12, 2002
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From Vitamin A derivatives (retinoids) are potent
regulators of cell proliferation and differentiation. Retinoids inhibit
the function of the oncogenic AP-1 and
The Role of Cadherin,
-Catenin, and AP-1 in Retinoid-regulated
Carcinoma Cell Differentiation and Proliferation*
§,§,,
The Lombardi Cancer Research Center and the
Departments of Oncology and Cell Biology, Georgetown University
School of Medicine, Washington, D. C. 20007 and the ¶ Division of
Medical Oncology, Department of Medicine, University of Texas Health
Science Center at San Antonio, San Antonio, Texas 78284
-catenin/TCF pathways and
also stabilize components of the adherens junction, a tumor suppressor
complex. When treated with retinoic acid (RA), the breast cancer cell
line, SKBR3, undergoes differentiation and reduction in cell
proliferation. The present work demonstrates that in SKBR3 cells, which
exhibit high AP-1 activity, RA-regulation of cadherin expression and
function, but not changes in AP-1 (or -catenin/TCF) signaling, is
responsible for the epithelial differentiation. However, cadherin
function and recruitment of -catenin to the membrane is not required
for RA to regulate DNA synthesis in these cells. RA also reduces the activity of an AP-1 and TCF-sensitive cyclin D1 reporter in SKBR3 cells
in a manner that is independent of the TCF site. In contrast, in SW480
cells, which have high levels of -catenin/TCF signaling, the
activity and retinoid responsiveness of the cyclin D1 promoter was
markedly inhibited by mutation of the TCF site. These data indicate
that the remarkably broad effects of RA on the growth and
differentiation of many different epithelial cancers may well be
explained by the ability of RA to differentially regulate the activity
of RAR/RXR, AP-1, and -catenin/TCF pathways.
*
This work was supported by grants from the National
Institutes of Health, the Department of Defense (to S. W. B. and
M. P.), and the American Association of Cancer Research-Bristol Myers Squibb Fellowship in Translation Colon Cancer Research (to S. S.).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: E415 The Research
Building, Georgetown University Medical Center, 3970 Reservoir Rd. NW,
Washington, DC 20007. Tel.: 202-687-1813; Fax: 202-687-7505; E-mail:
byerss@georgetown.edu.
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