Adams, David S.
University of Massachusetts Medical Center
The purpose of this project was to determine whether protein Mdm2, a p53 regulator previously shown to interact with MdmX, is required for the p53-independent role of MdmX in genome stabilization and suppression of cell transformation in vitro. Triple knock-out (TKO) cells lacking p53, Mdm2, and MdmX were transfected with an MdmX expression plasmid. Compared to control cells, TKO cells ectopically expressing MdmX show decreased cell proliferation, a longer cell cycle, increased chromosome numbers and bipolar mitotic spindles, and decreased foci formation. Thus, MdmX, even in the absence of Mdm2, plays a role in genome stability and proliferation. This is crucial to consider in regards to potential cancer treatments aimed to suppress Mdm2 and/or MdmX in order to reactivate p53.
Worcester Polytechnic Institute
Humanities and Arts
Major Qualifying Project
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Biology and Biotechnology