Enhanced c-fos expression after intracellular iron deprivation.
Intracellular iron deprivation by deferoxamine treatment, which leads to cells arrest in the S phase, enhanced c-fos expression in the neuroblastoma cell line, IMR32. The c-fos expression of iron deprived cells retained its response to stimulation by TPA, and cytosolic PKC activity did not decline after iron deprivation. The data suggest that PKC was not down-regulated. Creatine kinase activity also remained constant in the cytosol of iron deprived cells, indicating intact cellular function. Iron deprivation may activate the growth-related oncogene, c-fos, through some means other than the PKC pathway.
Fukuchi
K
K
Showa University, School of Medicine, Department of Clinical Pathology, Tokyo, Japan.
Tomoyasu
S
S
Watanabe
K
K
Watanabe
H
H
Takagi
Y
Y
Tsuruoka
N
N
Gomi
K
K
D003402:Creatine Kinase / Q000378:metabolism; D003600:Cytosol / Q000201:enzymology; D003676:Deferoxamine / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects; D016762:Genes, fos; D007501:Iron / Q000502:physiology*; D009447:Neuroblastoma / Q000473:pathology; D011493:Protein Kinase C / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis* / Q000235:genetics; D015398:Signal Transduction / Q000187:drug effects; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014407:Tumor Cells, Cultured / Q000187:drug effects
D016760:Proto-Oncogene Proteins c-fos; D007501:Iron; D011493:Protein Kinase C; D003402:Creatine Kinase; D003676:Deferoxamine; D013755:Tetradecanoylphorbol Acetate