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Blood, 1 August 2002, Vol. 100, No. 3, pp. 982-990
NEOPLASIA
Regulation of leukemic cell adhesion, proliferation, and survival
by  -catenin
Eun Joo Chung,
Sang-Gu Hwang,
PhuongMai Nguyen,
Sunmin Lee,
Jung-Sik Kim,
Jin Woo Kim,
Pierre A. Henkart,
Donald P. Bottaro,
Lilian Soon,
Paolo Bonvini,
Su-Jae Lee,
Judith E. Karp,
Ho Jung Oh,
Jeffrey S. Rubin, and
Jane B. Trepel
From the Medical Oncology Clinical Research Unit and
Developmental Therapeutics Program; Experimental Immunology Branch; and
Laboratory of Cellular and Molecular Biology; all of the National
Cancer Institute, National Institutes of Health, Bethesda, MD; and
Greenebaum Cancer Center, University of Maryland, Baltimore.
In epithelial cells  -catenin plays a critical role as a
component of the cell-cell adhesion apparatus and as a coactivator of
the TCF/LEF (T-cell transcription factor/lymphoid enhancer binding
factor) family of transcription factors. Deregulation of -catenin
has been implicated in the malignant transformation of cells of
epithelial origin. However, a function for -catenin in hematologic
malignancies has not been reported. -Catenin is not detectable in
normal peripheral blood T cells but is expressed in T-acute
lymphoblastic leukemia cells and other tumor lines of hematopoietic
origin and in primary lymphoid and myeloid leukemia cells. -Catenin
function was examined in Jurkat T-acute lymphoblastic leukemia cells.
Overexpression of dominant-negative -catenin or dominant-negative
TCF reduced -catenin nuclear signaling and inhibited Jurkat
proliferation and clonogenicity. Similarly, these constructs inhibited
proliferation of K562 and HUT-102 cells. Reduction of -catenin
expression with -catenin antisense down-regulated adhesion of Jurkat
cells in response to phytohemagglutinin. Incubation of Jurkat cells
with anti-Fas induced caspase-dependent limited proteolysis of
-catenin N- and C-terminal regions and rapid redistribution of
-catenin to the detergent-insoluble cytoskeleton, concomitant with a
marked decline in nuclear -catenin signaling. Fas-mediated apoptosis
was potentiated by inhibition of -catenin nuclear signaling. The
data suggest that -catenin can play a significant role in promoting
leukemic cell proliferation, adhesion, and survival.
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