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Blood, 15 June 2001, Vol. 97, No. 12, pp. 3890-3895
NEOPLASIA
Epithelial membrane protein 2, a 4-transmembrane protein that
suppresses B-cell lymphoma tumorigenicity
Chun-Xiang Wang,
Madhuri Wadehra,
Bernard C. Fisk,
Lee Goodglick, and
Jonathan Braun
From the Department of Pathology and Laboratory
Medicine, Jonsson Comprehensive Cancer Center, and Molecular Biology
Institute, University of California Los Angeles, Los Angeles, CA.
A murine homologue of the epithelial membrane protein 2 (EMP2) gene was identified in a search for genes
associated with B-cell lymphoma tumorigenicity by using suppression
subtractive hybridization. Expression of EMP2 messenger RNA in primary
mouse tissues was limited to certain epithelial cell types and the
peritoneal lymphoid compartment. EMP2 was expressed in the
poorly tumorigenic DAC B-lymphoma cell line but was significantly
down-regulated in a subline selected for in vivo tumor formation in
Balb/c mice. Recombinant restoration of EMP2 expression in
the subline suppressed its tumorigenicity, suggesting that loss of
EMP2 was a causal factor in the malignant phenotype.
Recombinant overexpression of EMP2 was studied in B lymphoma and NIH3T3 cells. EMP2 in both cell types induced
cell death on serum deprivation. EMP2-induced cell death
correlated with the expression level of EMP2 protein and was prevented
by caspase inhibitors Z-VAD and Z-DEVD. These findings for the
first time describe an apoptotic effect of a GAS3
family gene in lymphocytes. They also suggest that EMP2 may
influence B-lymphoma tumorigenicity through a functional tumor
suppressor phenotype.
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