| First Author | Hirota T | Year | 2005 |
| Journal | Oncogene | Volume | 24 |
| Issue | 13 | Pages | 2229-35 |
| PubMed ID | 15688018 | Mgi Jnum | J:97161 |
| Mgi Id | MGI:3574688 | Doi | 10.1038/sj.onc.1208409 |
| Citation | Hirota T, et al. (2005) Transcriptional activation of the mouse Necl-5/Tage4/PVR/CD155 gene by fibroblast growth factor or oncogenic Ras through the Raf-MEK-ERK-AP-1 pathway. Oncogene 24(13):2229-35 |
| abstractText | Necl-5/Tage4/poliovirus receptor/CD155 is the poliovirus receptor and upregulated in rodent and human carcinoma. We have recently shown that mouse Necl-5 is upregulated by an oncogenic Ki-Ras (V12Ki-Ras) in NIH3T3 cells and enhances cell movement induced by growth factors, including platelet-derived growth factor and fibroblast growth factor (FGF), in an integrin alpha(v)beta(3)-dependent manner in wild type and V12Ki-Ras-transformed NIH3T3 cells. In addition, it enhances the growth factor-induced cell proliferation. We examined here how mouse Necl-5 was upregulated by V12Ki-Ras in NIH3T3 cells. Expression of the luciferase reporter gene fused to the Necl-5 promoter was induced by V12Ki-Ras in NIH3T3 cells. This induction was mediated through the Raf-MEK-ERK pathway. The Necl-5 promoter has an AP-1-binding site and this site was required for the V12Ki-Ras-induced activation of the Necl-5 promoter. Expression of the luciferase reporter gene fused to the Necl-5 promoter was also induced by FGF through the Raf-MEK-ERK-AP-1 pathway in NIH3T3 cells. These results indicate that the expression of mouse Necl-5 is induced by FGF or V12Ki-Ras through the Raf-MEK-ERK-AP-1 pathway. |
