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J Biol Chem, Vol. 275, Issue 5, 3438-3445, February 4, 2000

Expression of the AML-1 Oncogene Shortens the G1 Phase of the Cell Cycle*

David K. StromDagger §, John NipDagger §par , Jennifer J. WestendorfDagger §, Bryan LinggiDagger §, Bart LutterbachDagger §**, James R. DowningDagger Dagger , Noel LennyDagger Dagger §§, and Scott W. HiebertDagger §¶¶

From the Dagger  Departments of Biochemistry and Medicine and the § Vanderbilt-Ingram Cancer Center, Vanderbilt University School of Medicine, Nashville, Tennessee 37232 and Dagger Dagger  Department of Pathology and the §§ Department of Tumor Cell Biology, St. Jude Children's Research Hospital, Memphis, Tennessee 38105

The AML-1-encoded transcription factor, AML-1B, regulates numerous hematopoietic-specific genes. Inappropriate expression of AML-1-family proteins is oncogenic in cell culture systems and in mice. To understand the oncogenic functions of AML-1, we established cell lines expressing AML-1B to examine the role of AML-1 in the cell cycle. DNA content analysis and bromodeoxyuridine pulse-chase studies indicated that entry into the S phase of the cell cycle was accelerated by up to 4 h in AML-1B-expressing 32D.3 myeloid progenitor cells as compared with control cells or cells expressing E2F-1. However, AML-1B was not able to induce continued cell cycle progression in the absence of growth factors. The DNA binding and transactivation domains of AML-1B were required for altering the cell cycle. Thus, AML-1B is the first transcription factor that affects the timing of the mammalian cell cycle.

* This work was supported by National Institutes of Health (NCI) Grants RO1 AG13726, RO1-CA64140, RO1-CA77274 (to S. W. H.), and F32 CA77167 (to J. J. W.), by NCI Center Grant CA68485, and by the Vanderbilt-Ingram Cancer Center.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.

Present address: Dept. of Biology, University of South Carolina, Aiken, SC 29801.

par A Special Fellow of the Leukemia Society of America (3827-99).

** A Fellow of the Leukemia Society of America (5669-99).

¶¶ To whom correspondence should be addressed: Dept. Of Biochemistry, Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Medical Research Building II, Rm. 512, 23rd and Pierce, Nashville, TN 37232. Tel.: 615-936-3582; Fax: 615-936-1790; E-mail: scott.hiebert@mcmail.vanderbilt.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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