ATHENS, Ga., Oct. 26 (UPI) -- Ovarian cancer can become more difficult to treat because of resistance to chemotherapy, however researchers at the University of Georgia have found the gene and protein it helps express that cause resistance, which may lead to better methods of treatment.
Most women treated for ovarian cancer have tumors come back, 85 percent are more aggressive and chemoresistant, because of a genetic change in their cancer's cells.
The researchers found a protein called RGS10, when activated by mTOR gene causes the drugs to ineffective. They think that keeping this protein from being turned off -- which is what causes chemotherapy to be ineffective -- could help the drugs work better.
"Depending on the expression levels of RGS10, the chemotherapy for ovarian cancer is more or less effective," said Shelley Hooks, an associate professor at UGA, in a press release. "If there were a way to reverse silencing of the RGS10 protein, then we could potentially restore sensitivity to drugs," she explained. "It would mean a better chance of survival for women with ovarian cancer."
Related
RGS proteins are involved with cancer initiation and progression. While studying this, Hooks and Mandi Murph, also an associate professor at UGA, found RGS10 is "basically an off switch." When the protein is deactivated by the mTOR gene in cancer cells, they can survive chemotherapy.
The researchers manipulated levels of RGS10 in ovarian cancer cells and tested several common chemotherapy drugs, finding they were more effective the more RGS10 had been expressed in cells.
RGS10 is epigenetically silenced, the researchers said, so external or environmental factors, rather than genetics, can turn the protein off.
"If there were a way to reverse silencing of the RGS10 protein, then we could potentially restore sensitivity to drugs," Hooks said. "It would mean a better chance of survival for women with ovarian cancer."
The study is published in Future Medicinal Chemistry.
