Transformation stimulates glucose transporter gene expression in the absence of protein kinase C.
The rat brain glucose transporter (GT) gene is rapidly activated coincident with the initiation of growth in response to oncogenic transformation or the addition of growth factors to quiescent fibroblasts. The latter response has been shown to be mediated by protein kinase C-dependent and-independent pathways. We studied the role of protein kinase C in the transformation-induced activation of the GT gene. Transformation of fibroblasts by either the v-fps or the Ki-ras oncogene rapidly increased the levels of GT mRNA. Either viral oncogene remained capable of stimulating the GT gene after depletion of cellular protein kinase C by prolonged pretreatment of fibroblasts with phorbol 12-myristate 13-acetate. These data indicate that protein kinase C is not required for the rapid activation of gene transcription by oncogenic transformation.
Hiraki
Y
Y
Department of Cellular and Molecular Physiology, Harvard Medical School, Boston, MA 02115.
Garcia de Herreros
A
A
Birnbaum
M J
MJ
D000818:Animals; D001921:Brain / Q000378:metabolism; D002460:Cell Line; D002471:Cell Transformation, Neoplastic; D005786:Gene Expression Regulation; D011905:Genes, ras; D006801:Humans; D007700:Kinetics; D009004:Monosaccharide Transport Proteins / Q000235:genetics*; D009857:Oncogenes; D011493:Protein Kinase C / Q000378:metabolism*; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics; D051381:Rats; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014158:Transcription, Genetic
D009004:Monosaccharide Transport Proteins; D012333:RNA, Messenger; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate