The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1999/2/501/ $5.00
The Journal of Experimental Medicine, Volume 189, Number 3, February 1, 1999 501-508

Articles

Growth Inhibition and Apoptosis Due to Restoration of E2A Activity in T Cell Acute Lymphoblastic Leukemia Cells

Steven T. Park*, Garry P. Nolan§, and Xiao-Hong Sun{ddagger}

From the * Department of Cell Biology and the {ddagger} Department of Cell Biology and Kaplan Cancer Center, New York University Medical Center, New York 10016; and the § Department of Molecular Pharmacology and Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, California 94305

Two models have been proposed for the molecular mechanism by which the Tal1 oncogene causes T cell acute lymphoblastic leukemia (T-ALL). The activation model suggests that Tal1 as heterodimers with the E2A transcription factor activates the expression of oncogenes. The inhibition model postulates that Tal1 interferes with the tumor-suppressing function of E2A. In the Jurkat T cell line, originally derived from a patient with T-ALL, Tal1 is complexed with E2A proteins and the transcriptional activity of E2A is very low. When E2A activity was restored by expressing an E2A–Tal1 fusion protein, E-T/2, the Jurkat cells underwent growth arrest and subsequently apoptosis, thus supporting the inhibition model and suggesting that E2A loss may contribute to leukemic progression.

Key Words: Tal1 • E2A • apoptosis • growth inhibition • leukemogenesis

Address correspondence to Xiao-Hong Sun, Department of Cell Biology and Kaplan Cancer Center, New York University Medical Center, 550 First Ave., New York, NY 10016. Phone: 212-263-6916; Fax: 212-263-8139; E-mail: sunx01{at}mcrcr.med.nyu.edu

Abbreviations used: bHLH, basic helix-loop-helix; BrdU, bromodeoxyuridine; EMSA, electrophoretic mobility shift assay; GFP, green fluorescent protein; PI, propidium iodide; T-ALL, T cell acute lymphoblastic leukemia; zVAD, zVAD-fluoromethylketone.


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