| First Author | Richard S | Year | 2008 |
| Journal | Oncogene | Volume | 27 |
| Issue | 4 | Pages | 548-56 |
| PubMed ID | 17621265 | Mgi Jnum | J:132092 |
| Mgi Id | MGI:3775127 | Doi | 10.1038/sj.onc.1210652 |
| Citation | Richard S, et al. (2008) Sam68 haploinsufficiency delays onset of mammary tumorigenesis and metastasis. Oncogene 27(4):548-56 |
| abstractText | The Src-associated substrate in mitosis Sam68 is a KH type RNA-binding protein known to be a substrate of numerous tyrosine kinases, and often referred to as a STAR (signal transduction activator of RNA) protein. Herein, we observed that Sam68-null mice display mammary gland and the uterine development defects. Moreover, we report that Sam68 haploinsufficiency impedes mammary tumor onset in vivo driven by the potent mammary-targeted polyoma middle T-antigen (MMTV-PyMT) oncogene. The effect was cell autonomous as the Sam68 knockdown in PyMT-transformed cell lines also delayed tumorigenesis and metastasis formation in nude mice. Interestingly, tumor extracts isolated from PyMT/Sam68(+/-) mice compared with PyMT/Sam68(+/+) mice contained activated Src and FAK kinases. These findings suggest that Sam68 may be a modulator of tyrosine kinase activity in vivo and a signaling requirement for mammary tumorigenesis and metastasis. |
