Butyrate-induced increase in neuron-specific enolase and ornithine decarboxylase in anaplastic glioma cells.
Butyrate treatment results in the rapid formation of processes on F98 anaplastic glioma cells. The morphological differentiation occurs more rapidly and to a greater extent than that induced by nerve growth factor (NGF). The incorporation of [3H]thymidine is virtually stopped 1 day after treatment of F98 cells with sodium butyrate. Butyrate also caused a large increase in ornithine decarboxylase activity in F98 cells between 6 and 12 h after treatment. This was inhibited by both cycloheximide and actinomycin-D. NGF did not cause these effects. Butyrate also caused an increase in neuron-specific enolase (NSE) content in F98 cells. This effect appeared to be specific for butyrate. Since NSE induction is characteristic only of neurons and neuroendocrine cells, this finding indicates that butyrate is capable of inducing biochemical differentiation along neuronal lines in undifferentiated glioma cells.
D000818:Animals; D002087:Butyrates / Q000494:pharmacology*; D002262:Carboxy-Lyases / Q000096:biosynthesis*; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000187:drug effects; D002478:Cells, Cultured; D004790:Enzyme Induction / Q000187:drug effects; D005910:Glioma / Q000201:enzymology*; D009374:Neoplasms, Experimental / Q000201:enzymology; D009955:Ornithine Decarboxylase / Q000096:biosynthesis*; D010751:Phosphopyruvate Hydratase / Q000096:biosynthesis*; D051381:Rats
D002087:Butyrates; D002262:Carboxy-Lyases; D009955:Ornithine Decarboxylase; D010751:Phosphopyruvate Hydratase