Resume

• The interferon inducible Myxovirus (influenza virus) resistance A (MxA) is considered as a key mediator of the interferon-induced antiviral response. Mx proteins contain the typical GTP-binding motif and show significant homology to dynamin family of GTPases. Strong interaction of MxA with tubulin suggests that Mx proteins could be involved in mitosis. Studies have shown that MxA inhibit tumor motility/metastasis and virus induced apoptosis. However

  the clear association between MxA expression and cancer remains unknown. Meta-analysis suggested that MxA expression was inversely correlated with prostate cancer (PCa). In this study

  we demonstrate the expression MxA in PCa and its functional significance on the cancer phenotype. Loss of MxA expression results in increased metastasis and decreased sensitivity to Docetaxel suggesting that MxA expression could determine the outcome of chemo-therapeutic treatment. Additional studies will be required to fully establish the cross-talk between androgen receptor-IFN pathway in regulating MxA expression in the normal prostate and prostate cancer.

  Interferon inducible antiviral MxA is inversely associated with prostate cancer and regulates cell cycle

  invasion and Docetaxel induced apoptosis.

  The myxovirus resistance A (MxA) gene -88G>T single nucleotide polymorphism is associated with prostate cancer

  Shanora G.

  Brown

  Ph.D.

  South Carolina State University

  Assistant Professor of Biology and Bioengineering Sciences

  Bachelor’s Degree

  Biology

  General

  Clark Atlanta University

  Doctor of Philosophy (Ph.D.)

  Molecular Biology