| First Author | D'Artista L | Year | 2016 |
| Journal | Oncotarget | Volume | 7 |
| Issue | 16 | Pages | 21786-98 |
| PubMed ID | 26943576 | Mgi Jnum | J:277127 |
| Mgi Id | MGI:6317127 | Doi | 10.18632/oncotarget.7846 |
| Citation | D'Artista L, et al. (2016) Pin1 is required for sustained B cell proliferation upon oncogenic activation of Myc. Oncotarget 7(16):21786-98 |
| abstractText | The c-myc proto-oncogene is activated by translocation in Burkitt's lymphoma and substitutions in codon 58 stabilize the Myc protein or augment its oncogenic potential. In wild-type Myc, phosphorylation of Ser 62 and Thr 58 provides a landing pad for the peptidyl prolyl-isomerase Pin1, which in turn promotes Ser 62 dephosphorylation and Myc degradation. However, the role of Pin1 in Myc-induced lymphomagenesis remains unknown. We show here that genetic ablation of Pin1 reduces lymphomagenesis in Emu-myc transgenic mice. In both Pin1-deficient B-cells and MEFs, the proliferative response to oncogenic Myc was selectively impaired, with no alterations in Myc-induced apoptosis or mitogen-induced cell cycle entry. This proliferative defect wasn't attributable to alterations in either Ser 62 phosphorylation or Myc-regulated transcription, but instead relied on the activity of the ARF-p53 pathway. Pin1 silencing in lymphomas retarded disease progression in mice, making Pin1 an attractive therapeutic target in Myc-driven tumors. |
