Signaling Components of the Anti-Tumor Hormone Somatostatin in Breast Cancer Cells
Abstract
The neuropeptide somatostatin is an important regulatory hormone that is widely distributed throughout the body. Somatostatin's actions are primarily inhibitory, and recently, it has been utilized as an antiproliferative agent against several tumor types, including breast neoplasms. Experimentally and clinically, somatostatin can inhibit breast cancer cell growth, possibly by inhibiting the secretion of growth factors, or by acting directly on the cells themselves to induce programmed cell death, or apoptosis. Despite increased clinical use, the mechanism(s) by which somatostatin acts to control breast cancer cell growth remain largely unknown. In this annual progress report, I describe studies performed on MDA23l cells, which show a robust response to somatostatin with regard to growth factor stimulation of the mitogen activated protein kinase, ERK1/2 (or MAPK). The activity of downstream components of the ras/raf/MAPK pathway, the Ets transcription factors, Ets- 1 and Elk- 1 are also inhibited by somatostatin. Furthermore, I show preliminary data indicating that another signaling pathway, the jun n-terminal kinase (JNK) pathway may be activated in response to somatostatin. . Together, these results begin to explain somatostatin's ability to inhibit cell growth and induce apoptosis in breast cancer. Furthermore, identification of these target pathways defines functional assays by which the efficacy of future anti-cancer drugs can be tested.
Document Details
- Document Type
- Technical Report
- Publication Date
- Oct 01, 1999
- Accession Number
- ADA386620
Entities
People
- Aurth Gutlerrez-hartman
- John Tentler
Organizations
- University of Colorado Health