SAT-530 ROS Level Regulation of Neural Cancer Stem Cells

Saturday, October 13, 2012: 9:40 PM
Hall 4E/F (WSCC)
Angelica Juarez , Neuroscience, University of California, Los Angeles, Los Angeles, CA
Janel Le Belle, PhD , University of California, Los Angeles, Los Angeles, CA
Harley Kornblum, MD, PhD , The Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA
Levels of reactive oxygen species (ROS) in neural stem cells (NSCs) can regulate cell proliferation, self-renewal and neurogenesis. The levels of ROS in NSCs are dependent on the enzyme nicotinamide adenine dinucleotide phosphate-oxidase (NOX). Previous studies have indicated the existence of cancer stem cells that initiate tumors and share many similarities with normal stem cells. Although it has been observed that most cancer cells show an increased level of NOX-generated ROS, the functional role that ROS plays in these cancer cells has not been determined. Therefore, we are investigating the role that NOX-generated ROS plays in neural cancer stem cell function. Two main questions are how the inhibition of the NOX enzyme affects the cancer cells’ proliferation, and how the cells respond after being released from this inhibition. We are currently examining the effects of different ROS levels on various neural cancer cell lines that originated from glial brain tumors obtained from patients after surgical resection. Cell culture assays of self-renewal and western blots will be performed to observe the signaling pathways that are activated in the cells due to changes in cellular ROS, such as phospho-AKT and phospho-S6, which play key roles in cell proliferation. By studying the activation of these pathways, we will be able to determine the differences caused by ROS in cancer stem cells compared to normal NSCs, which will contribute to developing new targets for glioblastoma cancer treatment.