HOUSTON - Researchers have identified a pivotal protein in a cellular transformation that makes a cancer cell more resistant to treatment and more capable of growing and spreading, making it an inviting new target for drug development.
Additionally, the international team led by scientists at The University of Texas MD Anderson Cancer Center found the cancer drug sunitinib potentially has a new role in treating triple-negative, claudin-low breast cancer, a particularly resistant version of a type of cancer that is already difficult to treat.
"We found that FOXC2 lies at the crossroads of the cellular properties of cancer stem cells and cells that have undergone epithelial to mesenchymal transition (EMT), a process of cellular change associated with generating cancer stem cells," said senior author Sendurai Mani, Ph.D., assistant professor in MD Anderson's Department of Translational Molecular Pathology and co-director of the Metastasis Research Center.
Cancer stem cells are fewer in number than other tumor cells, yet research has tied them to cancer progression and resistance to treatment. Abnormal activation of the epithelial to mesenchymal transition can create cancer stem cells, Mani noted.
Sunitinib stifles growth of cancer stem cells
"There are multiple molecular pathways that activate EMT," Mani said. "We found many of these pathways also activate FOXC2 expression to launch this transition, making FOXC2 a potentially efficient check point to block EMT from occurring," Mani said.
Research uncovering this connection, published in the journal Cancer Research, focused on cell line and mouse model experiments. The next important step will be to assess the expression and activity of FOXC2 in human tumor samples, Mani said.
In the meantime, sunitinib, known commercially as Sutent and approved by the U.S. Food and Drug Administration for three other cancers, provides interesting, more i
|Contact: Scott Merville|
University of Texas M. D. Anderson Cancer Center