Nucleic Acids Research, 2002, Vol. 30, No. 20 4489-4499
© 2002 Oxford University Press
Gene expression of TPA induced differentiation in HL-60 cells by DNA microarray analysis
Laboratory for Cancer Research, Department of Chemical Biology, College of Pharmacy, Rutgers, The State University of New Jersey, Piscataway, NJ 08854-8020, USA, 1 The Cancer Institute of New Jersey, UMDNJ-Robert Wood Johnson Medical School, 195 Little Albany Street, Room 2012, New Brunswick, NJ 08901, USA, 2 Department of Molecular Genetics and Microbiology, and The Center for Advanced Biotechnology and Medicine, UMDNJ-Robert Wood Johnson Medical School, Piscataway, NJ 08854, USA and 3 Biochip Technology Center, Argonne National Laboratories, Argonne, Illinois, IL 60439, USA
*To whom correspondence should be addressed at present address: Laboratory for Cancer Research, Department of Chemical Biology, College of Pharmacy, Rutgers University, 164 Frelinghuysen Road, Piscataway, NJ 08854-0789, USA. Tel: +1 732 445 3400; Fax: +1 732 445 0687; Email: chinkv{at}rci.rutgers.edu
The tumor promoter 12-O-tetradecanoylphorbol-13-acetate (TPA) is a potent inducer of differentiation in human promyelocytic leukemia cells. Recently, TPA has been successfully administered to patients with myelocytic leukemia and has produced therapeutic effects that led to temporary remission. These studies demonstrated the potential efficacy of TPA in cancer chemotherapy. We now seek to understand the biological effects and molecular mechanisms of differentiation in response to TPA treatment in leukemia cells by expression profiling using DNA microarray. Our results show distinct temporal and coordinated gene changes that are consistent with differentiation and activation of multiple biochemical pathways in HL-60 cells exposed to TPA. Alterations of gene expression in HL-60 cells include various transcription factors, cytokines and protein markers that are consistent with the induction of differentiation elicited by TPA. These temporal patterns of gene expression were abolished or greatly diminished in an HL-60 derived TPA- resistant variant cell line (HL-525), thus revealing transcriptional and consequential biochemical changes that may be required for TPA-induced differentiation. In addition, certain genes were upregulated by TPA in TPA-resistant HL-525 cells but not in TPA-sensitive HL-60 cells suggesting that these genes may play a role in the resistant pheno type. These patterns of gene expression may be important for predicting response to TPA.
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