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Motor protein may offer promise in ovarian cancer treatment
Date:4/26/2011

A motor regulatory protein can block human ovarian tumor growth, leading to eventual cancer cell death and possible new therapies to treat the disease, according to Penn State College of Medicine researchers.

Among U.S. women, an estimated 21,880 new cases and 13,850 deaths occurred in 2010 from epithelial ovarian cancer, one of the most common forms of ovarian cancer and the most lethal gynecologic cancer in women.

Previously, Kathleen M. Mulder, Ph.D., professor, biochemistry and molecular biology, along with members of her laboratory, learned that km23-1 -- a protein -- is defective in nearly half of all ovarian cancer patients. In the current study, researchers induced over-expression of km23-1 in human ovarian cancer cells placed in mice, causing the cells to produce large amounts of the normal protein.

km23-1 is a subunit of dynein, a motor protein that transports cargo along paths in the cell called microtubules. The dynein motor has many jobs in the cell, including major roles in cell division.

"Although microtubule-binding agents, such as the drug paclitaxel, are being used in the treatment of ovarian cancer, drug resistance has significantly limited their efficacy," Mulder said. "It is critical to develop novel, targeted therapeutics for ovarian cancer. Motor protein regulatory agents may offer promise for providing improved efficacies with reduced side effects in the treatment of ovarian cancer and other human malignancies."

Nageswara Pulipati, Ph.D., postdoctoral fellow in Mulder's lab, said, "We used a method to cause the tumors to express high levels of normal km23-1, but only in the experimental group of mice. Compared to the control group, the tumors were much smaller when km23-1 was over-expressed."

Findings were reported online (http://onlinelibrary.wiley.com/doi/10.1002/ijc.25954/abstract) and will appear in an upcoming edition of The
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Contact: Matt Solovey
msolovey@hmc.psu.edu
717-531-8606
Penn State
Source:Eurekalert

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