A traffic cop protein in the cell may have an even more important role: transporting a messenger protein that tells components in the nucleus to stop cell growth. The discovery of this additional role may lead to diagnostic tools and earlier treatments for ovarian cancer.
A Penn State College of Medicine research team, led by Kathleen M. Mulder, Ph.D., professor of pharmacology, is studying the normal function of a protein called km23, the traffice cop protein, because the team previously found altered forms of the protein in 42 percent of tumor tissue samples taken from women with ovarian cancer.
No similar alterations were found in normal human tissues, suggesting that the km23 alterations may be a possible diagnostic indicator for development of ovarian cancer and that the km23 protein itself may be a possible target for cancer therapies.
km23 is part of the signaling system for a growth factor called TGF, which attaches to TGF receptors at the cell membrane. It activates km23 into action.
km23 acts like a traffic cop for specific proteins as they move in the cell on a highway called a microtubule. It is responsible for helping to match the right cellular cargo with the right motor complex to get the cargo to the correct destination when its needed. One of those precious cargoes is a TGF-signaling component that must get to the cell nucleus to turn on specific genes that help stop cell growth.
Alterations in the TGF signaling system are known to contribute to cancer, Mulder said. We have been searching for new components of this signaling system to determine whether they are also altered in cancer and contribute to its development. These components can then be used to design new treatment strategies for cancer once we understand how they normally function.
In the current study, Mulders team found that blocking km23 from doing its job in the TGF- signaling system disrupted the transport of the sig
Contact: Megan Manlove