Involvement of stress-activated protein kinase in the cellular response to 1-beta-D-arabinofuranosylcytosine and other DNA-damaging agents

Cell Growth Differ. 1995 Dec;6(12):1651-8.

Abstract

The cellular response to 1-beta-D-arabinofuranosylcytosine (ara-C) includes activation of Jun/AP-1, induction of c-jun transcription, and programmed cell death. The stress-activated protein (SAP) kinases stimulate the transactivation function of c-jun by amino terminal phosphorylation. The present work demonstrates that ara-C activates p54 SAP kinase. The finding that SAP kinase is also activated by alkylating agents (mitomycin C and cisplatinum) and the topoisomerase I inhibitor 9-amino-camptothecin supports DNA damage as an initial signal in this cascade. The results demonstrate that ara-C also induces binding of SAP kinase to the SH2/SH3-containing adapter protein Grb2. SAP kinase binds to the SH3 domains of Grb2, while interaction of the p85 alpha-subunit of phosphatidylinositol 3-kinase complex. The results also demonstrate that ara-C treatment is associated with inhibition of lipid and serine kinase activities of PI 3-kinase. The potential significance of the ara-C-induced interaction between SAP kinase and PI 3-kinase is further supported by the demonstration that Wortmannin, an inhibitor of PI 3-kinase, stimulates SAP kinase activity. The finding that Wortmannin treatment is also associated with internucleosomal DNA fragmentation may support a potential link between PI 3-kinase and regulation of both SAP kinase and programmed cell death.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Adaptor Proteins, Signal Transducing*
  • Androstadienes / pharmacology
  • Antimetabolites, Antineoplastic / toxicity*
  • Calcium-Calmodulin-Dependent Protein Kinases / metabolism*
  • Cell Line
  • Cytarabine / toxicity*
  • DNA Damage*
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • GRB2 Adaptor Protein
  • Glutathione Transferase / metabolism
  • Humans
  • JNK Mitogen-Activated Protein Kinases
  • Leukemia, Myeloid
  • Mitogen-Activated Protein Kinases*
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor) / metabolism
  • Protein Kinases / isolation & purification
  • Protein Kinases / metabolism*
  • Proteins / metabolism
  • Proto-Oncogene Proteins c-jun / isolation & purification
  • Proto-Oncogene Proteins c-jun / metabolism
  • Recombinant Proteins / biosynthesis
  • Recombinant Proteins / metabolism
  • Stress, Physiological
  • Tumor Cells, Cultured
  • Wortmannin
  • p38 Mitogen-Activated Protein Kinases
  • src Homology Domains

Substances

  • Adaptor Proteins, Signal Transducing
  • Androstadienes
  • Antimetabolites, Antineoplastic
  • Enzyme Inhibitors
  • GRB2 Adaptor Protein
  • GRB2 protein, human
  • Proteins
  • Proto-Oncogene Proteins c-jun
  • Recombinant Proteins
  • Cytarabine
  • Glutathione Transferase
  • Protein Kinases
  • Phosphatidylinositol 3-Kinases
  • Phosphotransferases (Alcohol Group Acceptor)
  • Calcium-Calmodulin-Dependent Protein Kinases
  • JNK Mitogen-Activated Protein Kinases
  • Mitogen-Activated Protein Kinases
  • p38 Mitogen-Activated Protein Kinases
  • Wortmannin