Discovery may lead to new cancer treatments, scientists say
THURSDAY, June 25 (HealthDay News) -- A protein called STAT3 plays a major role in the change of normal cells into cancerous cells, according to U.S. researchers, who say the finding could lead to new cancer treatments.
STAT3, which has a role in the cell nucleus regulating gene expression, is also present in the mitochondria of cells and regulates the electron transport chain in tumor cells, said the study's leader, David E. Levy, a professor of pathology and microbiology at New York University's Langone Medical Center.
Mitochondria -- the energy source in cells -- are known to be critical to tumor cell metabolism.
"These results open the possibility that inhibiting the mitochondrial function of STAT3 could be a promising cancer therapy in the future," Levy said in a news release from the university's medical school.
"By knowing this mitochondrial function is critical, it may be possible to design therapeutic strategies that specifically target this function while sparing the other functions of the protein, such as its ability to turn genes on," he explained. "Therefore, we would hope that inhibitors could be developed that would be highly specific for cancer cells."
Levy and his team made the discovery about the mitochondrial role of STAT3 by analyzing tumors caused by the Ras oncogene, which has been determined to be involved in many human cancers.
A report on the findings appears in the June 26 issue of Science.
"Future experiments will need to determine if a similar mitochondrial role for STAT3 is critical for other types of cancer as well," Levy said. "We'll also need a better understanding of the biochemical basis for the function of STAT3. For instance, we are trying to find out what STAT3 does in mitochondria, what enzymes and processes it regulates and how these processes differ in tumors compared to normal cells."
The U.S. National Cancer Institute has more about cancer.
-- Robert Preidt
SOURCE: NYU School of Medicine, news release, June 25, 2009
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