Pim-1, a Potential Participant in Breast Cancer
Abstract
Pim-l, a serine/threonine kinase involved in proliferation, differentiation and survival, is a protooncogene involved in cancers of hematopoietic origin. Once thought only to be expressed in hematopoietic cells, it also is expressed in many cell types including epithelial cells. It is therefore suspected that Pim-l may also play a role in promoting breast cancer. We are examining how Pim-l expression is regulated in mammary epithelial cells where a signaling pathway called the JAK2/Stat5a (Janus kinase 2/Signal transducer and activator of transcription 5a) pathway, is activated by hormones such as prolactin. This pathway is suspected to regulate pim-1 transcription. To date, wild type, constitutively active and dominant negative mutants of Stat5a have been made. Mammary epithelial cells have been treated with prolactin and a dose-dependent response has been observed which correlates to Stat5a phosphorylation state. It appears the three cell lines used, which differ in their progesterone and prolactin receptor levels, do not contain equal basal levels of Pim-l and do not respond identically to prolactin and progesterone stimulation. It is suspected that the ability of these hormones to regulate expression of Pim-l in mammary epithelial cells allows cells to survive and accumulate mutations resulting in a cell becoming cancerous.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jul 01, 2002
- Accession Number
- ADA408723
Entities
People
- Maria Meyer
- Nancy S. Magnuson
Organizations
- Washington State University