| First Author | Li N | Year | 2016 |
| Journal | Oncotarget | Volume | 7 |
| Issue | 44 | Pages | 71651-71659 |
| PubMed ID | 27690217 | Mgi Jnum | J:314988 |
| Mgi Id | MGI:6829307 | Doi | 10.18632/oncotarget.12305 |
| Citation | Li N, et al. (2016) The p53 status can influence the role of Sam68 in tumorigenesis. Oncotarget 7(44):71651-71659 |
| abstractText | The expression and activities of RNA binding proteins are frequently dysregulated in human cancer. Their roles, however, appears to be complex, with reports indicating both pro-tumorigenic and tumor suppressive functions. Here we show, using two classical mouse cancer models, that the role of KH-type RNA binding protein, Sam68, in tumor development can be influenced by the status of the p53 tumor suppressor. We demonstrate that in mice expressing wild type p53, Sam68-deficiency resulted in a higher incidence and malignancy of carcinogen-induced tumors, suggesting a tumor suppressive role for Sam68. In marked contrast, Sam68-haploinsufficiency significantly delayed the onset of tumors in mice lacking p53 and prolonged their survival, indicating that Sam68 accelerates the development of p53-deficient tumors. These findings provide considerable insight into a previously unknown relationship between Sam68 and the p53 tumor suppressor in tumorigenesis. |
