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Acceleration of Apoptosis in Transforming Growth Factor ß1-treated M1 Cells Ectopically Expressing B-myb

Laboratory of Genetics, National Cancer Institute, NIH, Bethesda, Maryland 20892

Inappropriate expression of genes involved in cell proliferation can result in altered regulation of apoptosis, a process of programmed cell death. Since B-myb has recently been implicated in the cell cycle progression we wanted to examine its role in the apoptotic process. For this purpose we used transforming growth factor ß1 (TGF-ß1)-treated M1 myeloid leukemia cell lines that continuously express murine B-myb. It was found that in cells overexpressing B-myb, TGF-ß1-induced apoptosis was accelerated as assessed by cell viability and DNA fragmentation into nucleosomal fragments. A DNA ladder was detected after 24 h of TGF-ß1 treatment in these cells, whereas it was not detected until after 36 h in the parental M1 cells. It was further determined by Northern blot analysis that this higher sensitivity of B-myb overexpressing clones was not due to a change in the expression of TGF-ß receptor type I or in the kinetics of the regulation of c-myc, c-myb, bcl-2, and/or bax.

¹ On leave from the Cancer Research Institute, Slovak Academy of Sciences, Bratislava, Slovakia.

² To whom requests for reprints should be addressed, at Laboratory of Genetics, Building 37, Room 2B04, National Cancer Institute, NIH, 37 Convent Drive, MSC 4255, Bethesda, MD 20892-4255.

Received 11/15/94. Accepted 12/19/94.

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