Department of Pharmacology Faculty

Dale Parker Suttle, Jr., Ph.D.

Dale Parker Suttle, Jr., Ph.D.

Associate Professor
Room 601G Molecular Sciences Building
Phone: 901-448-7810
Fax: 901-448-7847



  • Southern Nazarene University, Bethany, OK, B.S. 1970
  • University of Texas at Austin, Austin, TX, Ph.D. 1975 Biochemistry
  • Stanford University School of Medicine, Stanford, CA
    Postdoctoral Fellow 1975-78 Biochemistry

Research Interests

The double helical structure of the DNA molecule inside the cell must change it topology as the DNA is replicated and the chromosomes are segregated at cell division. DNA topoisomerase IIa is the enzyme required for making these changes in the topology of DNA. Topo IIa passes a double stranded DNA segment through a transient double strand break in a second DNA strand to modify the helical twist of the DNA molecule. This action of topo IIa is required at mitosis for the chromosomes to separate into the two daughter cells. The level of topo IIa protein in the cell is directly correlated with the cell proliferation rate and with the stage of the cell cycle. Topo IIa levels are highest just before the cell divides at mitosis. Because of the interaction of topo IIa with DNA in critical cellular functions, it is both a unique and a natural target for anticancer drugs that can inhibit cell growth or induce cell death.

DNA strand breaks caused by the action of topo IIa and drugs can induce the tumor suppressor protein p53, which causes a G1 cell cycle checkpoint arrest. The action of wild type p53 is to stop cell growth, providing time for DNA repair, and thus preventing development of tumor cells. If DNA damage is beyond repair, p53 promotes apoptosis or programmed cell death. Studies in our lab have indicated wild type p53 serves as a negative controlling factor for the regulation of topo IIa expression, preventing the required transcription factors from binding to specific sites in the topo IIa promoter. Similar inhibitory effects on the expression of topo IIa are seen when cells are treated with specific anticancer drugs. This drug-induced inhibition of topo IIa is seen in cells regardless of the presence of wild type p53 in the cells. Our present research efforts are to determine the factors and effects that modulate topoIIa gene expression in response to p53 induction and following treatment with anticancer drugs. In addition, our research will study the effect of topo IIa expression on the progression of the cell through the G2/M phase of the cycle, which may be distinct from the p53-dependent DNA-damage checkpoint. These studies of topo IIa regulation in normal and tumor cells will yield vital information for the effective use of the clinically important topo IIa-targeted anticancer drugs.


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