title: Butyrate induces an ectoMg2(+)-ATPase activity in Li-7A human hepatoma cells.
abstract: The human hepatoma cell line (Li-7A) possesses a high concentration of epidermal growth factor (EGF) receptors and exhibits ectoATPase activity in the presence of either MgATP or CaATP (Knowles: J. Cell. Physiol., 134:109-116, 1988). Growth for 96 hours in the presence of both EGF and cholera toxin or another cyclic AMP elevating agent induced an ectoATPase activity which was more active with CaATP and resistant to inhibition by the sulfydryl reagent, p-chloromercuriphenylsulfonate (pCMPS) (Knowles: Arch. Biochem. Biophys., 263: 264-271, 1988). In contrast, treatment of cells with butyrate, a short chain organic acid which can be derived from the analogue, dibutyryl cyclic AMP, resulted in a 4-7-fold increase of an ectoATPase which was more active with MgATP and highly sensitive to pCMPS inhibition. Maximal induction by butyrate required 48 hours and was dependent on butyrate concentration, but was independent of EGF and cyclic AMP elevating agents. Of six organic acids tested, butyrate was most effective in the induction of the ectoMg2(+)-ATPase. The increase in the ectoMg2(+)-ATPase activity could be prevented with actinomycin D and cycloheximide, indicating that both transcription and translation were necessary for induction. In addition to the induction of the ectoMg2(+)-ATPase, butyrate induced alkaline phosphatase activity, but had no effect on a third ectoenzyme 5'-nucleotidase. These data further support our proposal that two distinct ectoATPases exist in the plasma membrane of Li-7A hepatoma cells.
authors.affiliation: Department of Biology, Northeastern University, Boston, Massachusetts 02115.
authors.forename: S L
authors.initials: SL
authors.lastname: Murray
authors.forename: A F
authors.initials: AF
authors.lastname: Knowles
mesh_terms: D002731:4-Chloromercuribenzenesulfonate / Q000494:pharmacology; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D001693:Biological Transport, Active / Q000187:drug effects; D003994:Bucladesine / Q000494:pharmacology; D002087:Butyrates / Q000494:pharmacology*; D006528:Carcinoma, Hepatocellular / Q000201:enzymology*; D002455:Cell Division / Q000187:drug effects; D003513:Cycloheximide / Q000494:pharmacology; D003609:Dactinomycin / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004790:Enzyme Induction / Q000187:drug effects; D004815:Epidermal Growth Factor / Q000494:pharmacology; D005227:Fatty Acids / Q000494:pharmacology; D006801:Humans; D007700:Kinetics; D008113:Liver Neoplasms / Q000201:enzymology; D009363:Neoplasm Proteins / Q000096:biosynthesis; D013997:Time Factors; D014407:Tumor Cells, Cultured
chemical_list: D002087:Butyrates; D005227:Fatty Acids; D009363:Neoplasm Proteins; D003609:Dactinomycin; D002731:4-Chloromercuribenzenesulfonate; D004815:Epidermal Growth Factor; D003994:Bucladesine; D003513:Cycloheximide; D000251:Adenosine Triphosphatases