Mammalian Target of Rapamycin Regulates Cell Differentiation through STAT3-p63-Jagged-Notch Cascade, an article co-authored by Erxi Wu, NDSU assistant professor of pharmaceutical sciences, will be published by The Journal of Clinical Investigation. http://www.jci.org/
According to the authors, the receptor tyrosine kinase (RTK)-phosphatidylinositol 3-kinase (PI3K)-AKT-mammalian target of rapamycin (mTOR) pathway is one of the most frequently altered signaling networks in cancer, but the underlying mechanism leading to tumorigenesis by activated mTOR remains less clear.
This study led by collaborator Hongbing Zhang from China presents evidence demonstrating that mTOR complex 1 (mTORC1) is a positive regulator of Notch signaling, acting through up-regulation of the STAT3-p63-Jagged1 signaling cascade in mouse and human cells. In response to differential cues from mTOR, the authors discovered Notch serves as a molecular switch to shift the balance between cell proliferation and differentiation. "Components of the STAT3-p63-Notch axis are potential targets for the treatment of diseases such as cancers caused by hyperactive RTK-PI3K-AKT-mTOR signaling," Wu said. The Journal of Clinical Investigation is a top-tier venue for critical advances in biomedical research. The JCI combines a 2008 Impact Factor of 16.559 with immediate free access to its articles to produce an ideal home for authors seeking the widest possible audience for their most important work.