Changes in Reactive oxygen as a mechanism for NF-kb
Activation
Kenneth G Yancey, Craig Woodworth
Human Papilloma-Virus (HPV) causes over 99% of cervical cancers, the second leading cause of
death in women. Our long term goal is to examine whether HPV activates the transcription factor NF-kB.
Nf-kB activates many biological responses essential for carcinogenesis including proliferation,
vascularization, anti-apoptosis and chemoresistivity. Because of this importance there has been large scale
research into the pathways controlling the activation of NF-kB including reactive oxygen species (ROS).
ROS are free radicals produced by metabolic processes. They are vital to signal transduction and apoptosis
but can also cause cell stress and induce mutation. Our hypothesis is that ROS is an important factor for
inducing NF-kB in human cervical cells. Specifically we plan to elucidate the level in which ROS is
involved in NF-kB activation in cervical cells infected with HPV and cells which are being treated with the
growth inhibitory drug erlotinib. In this pursuit, we are currently quantifying different components in the
ROS regulation pathway such as super oxide dismutase (SOD) and catalase (Cat) as a result of hpv and
erlotinib treatment. Before we can make conclusions, we must optimize our SOD and CAT assays. In
addition, we need to develop a new hydrogen peroxide assay that has increased sensitivity. These
experiments are in progress. As we continue on we hope to expand our experiment using varying doses of
erlotinib and dose responses.