New pathway could present an intervention point for cancer treatmentA new cellular pathway leads to destruction of a protein that promotes growth of breast, prostate and similar cancers and could provide a new avenue through which to pursue treatment of such diseases, said a researcher at Baylor College of Medicine.
"It is another intervention point where one can now attack tumors. It's especially important for endocrine tumors such as those of the breast, prostate, ovary and pituitary gland," said Dr. Bert O'Malley, chair of the BCM department of molecular and cellular biology. O'Malley is senior author of a report on the research that appears in the current issue of the journal Cell and a faculty member in the College's Graduate School of Biomedical Sciences.
O'Malley and his colleagues concentrated their efforts on a powerful oncogene or cancer-promoting gene called the steroid receptor coactivator (SRC) 3 which is also a powerful promoter of tumor growth.
"In high concentrations, it drives the cells to relentless replications," O'Malley said.
However, studies in the laboratory showed that another molecule called REG-GAMMA takes SRC3 to the proteasome where it is destroyed.
"Because REG-GAMMA does this to SRC3, it is a tumor suppressor," said O'Malley.
In breast cancer, when levels of REG-GAMMA are low, SRC3 levels can be high, resulting in tumor growth, said O'Malley.
"This is an important pathway for SRC3 degradation that has never been described," said O'Malley. Other modes of taking proteins to the proteasome for destruction involve adding a molecule called ubiquitin and using energy.
"This molecule does not require ubiquitin or an energy source," he said. "It's a really strange and different molecule for that reason."
He and members of his laboratory plan to determine if the molecule controls similar proteins involved in tumor promotion as well.
Others members of the team that worked on the project include: Drs. Xiaotao Li, David M. Lonard, Sun Yun Jung, Anna Malovannaya, Qin Feng, Jun Qin, Sophia Y. Tsai and Ming-Jer Tsai.
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