Document 0052
 DOCN  M95B0052
 TI    Differences in sensitivity to induction of apoptosis among rat
       fibroblast cells transformed by HTLV-I tax gene or cellular nuclear
       oncogenes.
 DT    9511
 AU    Fujita M; Shiku H; Department of Oncology, Nagasaki University School of
       Medicine,; Japan.
 SO    Oncogene. 1995 Jul 6;11(1):15-20. Unique Identifier : AIDSLINE
       MED/95349926
 AB    The tax gene of human T lymphotropic virus type I has been implicated in
       the genesis of adult T cell leukemia (ATL). It has been reported that
       expression of tax induces neoplastic transformation in the rat
       fibroblast cell line Rat-1, and that co-expression with the ras gene can
       transform rat embryo fibroblasts. Possible activation of cellular
       oncogenes including c-myc and c-fos by tax has been implicated in these
       tax functions. In this study, comparative analysis of biological
       properties of tax and cellular nuclear oncogenes c-myc and c-fos was
       performed in Rat-1 cells. While all three oncogenes could transform
       Rat-1 cells, significant differences in the sensitivity to induction of
       apoptosis were observed between cells transformed with each oncogene.
       Induction of apoptosis by serum starvation was observed in
       tax-transfected Rat-1 cells but to a lesser extent than that in those
       transfected with c-myc or c-fos. In contrast, exposure to a DNA-damaging
       agent, etoposide, resulted in enhanced apoptotic death only in
       c-myc-transfected Rat-1 cells. Our findings indicate that the pathways
       for apoptosis induction may not be identical among these three
       oncogenes, and that the relatively low apoptosis-inducing activity and
       sufficient transforming capacity of tax might be associated with
       transformation of T cells and the low susceptibility of the transformed
       T cells (ATL cells) to chemotherapeutic agents.
 DE    Animal  Apoptosis/DRUG EFFECTS/*GENETICS  Cell Nucleus  Cell
       Transformation, Neoplastic/GENETICS  Cell Transformation, Viral/GENETICS
       Culture Media, Serum-Free  Etoposide/PHARMACOLOGY  Fibroblasts  *Genes,
       fos  *Genes, myc  Genes, pX/*GENETICS  Genes, p53  HTLV-I/*GENETICS
       Rats  JOURNAL ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).