UNC Lineberger’s Michael J. Emanuele, PhD, and colleagues have identified a key activator that can turn on FoxM1, a protein that drives expression of genes that help cells replicate and divide, a finding they published in the journal Molecular and Cellular Biology. They also discovered, paradoxically, that the activator for FoxM1 is also responsible for turning this protein off.
Researchers at the University of North Carolina Lineberger Comprehensive Cancer Center have identified some of the bad actors that can step on the gas to help drive cells to replicate and divide abnormally in ovarian cancer.
In a study published in the journal Molecular and Cellular Biology, researchers report that they’ve discovered a key activator that can turn on FoxM1, a protein that drives expression of genes that help cells replicate and divide. They also discovered, paradoxically, that the activator for FoxM1 is also responsible for turning this protein off.
The finding could help direct future lines of research that target this FoxM1 activator, which could lead to a possible therapeutic approach for ovarian cancer, the fifth leading cause of cancer death in women in the United States.
“If we can understand what tips the balance of the regulation of this protein, we might have an entry point for therapeutically inactivating FoxM1 by triggering its destruction,” said the study’s corresponding author Michael J. Emanuele, PhD, a UNC Lineberger member and assistant professor in the Department of Pharmacology.
Other authors include Xianxi Wang and Rjarshi Choudhury of UNC Lineberger; Anthony Arceci of UNC Lineberger and the UNC Curriculum in Genetics and Molecular Biology; Kelly Bird of the UNC Eshelman School of Pharmacy; Christine A. Mills, Jennifer L. Kernan and Albert Bowers of UNC Lineberger and the UNC Eshelman School of Pharmacy; and Chunxiao Zhou of UNC Lineberger and the Division of Gynecologic Oncology.
~except from full article on Lineberger Pathways – read the full article here