Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth.

摘要

The purpose of this research project was originally to characterize growth inhibitory effects of interleukin-4 (IL-4) in breast cancer cells and identify key signaling molecules that may be targets for future strategies to enhance the negative growth effects of IL-4. The original investigators have reported that IL-4-mediated growth inhibition is associated with increased apoptosis and that IL-4 activates two important signaling molecules, IRS-i and STAT6. Inhibition of IRS-i does not block IL-4-mediated growth effects while inhibition of STAT6 decreases IL-4-mediated growth inhibition and apoptosis. Additionally, over-expression of STAT6 mimics the effect of IL-4. Finally, the investigators examined the mechanism of INF gamma-mediated growth inhibition of breast cancer cells in vitro. In addition to the JAK-STAT pathway, INF gamma decreases breast cancer cell growth in p21 dependent and independent pathways. In conclusion, their research on the mechanism and signal transduction pathways of IL-4 in human breast cancer cells has resulted in numerous original and significant findings. As of 10/00, this grant entitled 'Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth' was transferred to Jill Ricono, a graduate student in the Department of Nephrology at the University of Texas Health Science Center at San Antonio where research focuses on the pathogenic mechanisms involved in kidney development and progression of renal disease; specifically, the effects of Platelet-derived growth factor (PDGF) on development and maturation of microvascular cells and their precursors in the metanephric kidney.