Abstract
The estrogen receptors ERα and ERβ have been implicated in the progression of a wide variety of cancers. The actions of ER are regulated by ER coregulator proteins, including proline-, glutamic acid-and leucine-rich-protein-1 (PELP1/MNAR). PELP1 has been shown to participate in both genomic and nongenomic functions of ER. The expression and localization of PELP1/MNAR are deregulated in a wide variety of tumors and have been implicated in the development of hormonal resistance in cancer cell lines. Emerging data suggest that PELP1/MNAR interacts with many proteins and activates several oncogenes, including Src kinase, phosphotidyl inositol 3 kinase (PI3K), and signal transducers and activators of transcription 3 (STAT3). These new results suggest that PELP1/MNAR may act as an oncogene as well as cooperating with other oncogenes. Thus, PELP1/MNAR may contribute to the tumorigenic potential of cancer cells by serving as a scaffolding protein that couples various signaling complexes with ER.
| Original language | English |
|---|---|
| Pages (from-to) | 91-96 |
| Number of pages | 6 |
| Journal | Histology and Histopathology |
| Volume | 22 |
| Issue number | 1-3 |
| State | Published - Jan 2007 |
| Externally published | Yes |
Keywords
- Coregulators
- Estrogen receptors
- Hormonal resistance
- MNAR
- PELP1