Skip to comments.Compound Used to Block Cholesterol Could Also Kill Breast Cancer, MU Researcher Finds
Posted on 02/22/2011 3:29:05 PM PST by decimon
COLUMBIA, Mo. A University of Missouri researcher believes there could be a new drug compound that could kill breast cancer cells. The compound might also help with controlling cholesterol.
Salman Hyder, the Zalk Endowed Professor in Tumor Angiogenesis and professor of biomedical sciences in the College of Veterinary Medicine and the Dalton Cardiovascular Research Center, and his research team discovered that a small molecule, Ro 48-8071, initially developed for controlling cholesterol synthesis dramatically destroys human breast cancer cells. This development was discovered as Hyders research team was investigating PRIMA-1, a drug that targets a common mutated gene in human breast cancer cells, and kills tumor cells.
During the course of the study, Xiaoquin Zou, an assistant professor in the MU Department of Physics and Astronomy, compared the chemistry of PRIMA-1 binding to thousands of proteins using a software program she developed called MDock. Hyder and Zou found that PRIMA-1 showed excellent binding properties to a protein called oxidosqualene cyclase, (OSC) that is known to be important for producing cholesterol. This led Hyders team to investigate whether known OSC inhibitors, such as Ro 48-8071, developed to stop cholesterol production, also killed breast cancer cells.
We had been working with PRIMA-1 for some time, and what we didnt quite understand is exactly how it killed tumor cells, Hyder said. With the current findings, we think its possible that one mechanism utilized by PRIMA-1 to kill cancer cells may include shutting down cholesterol synthesis, but we still dont know for certain if thats the case. What we do know is that Ro 48-8071 does stop cholesterol synthesis, and it proved to be just as effective in destroying cancer cells as PRIMA-1, without harming other normal breast cells, which is a big advantage.
(Excerpt) Read more at munews.missouri.edu ...
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