| First Author | Li F | Year | 2015 |
| Journal | Endocrinology | Volume | 156 |
| Issue | 1 | Pages | 48-57 |
| PubMed ID | 25343275 | Mgi Jnum | J:234890 |
| Mgi Id | MGI:5791049 | Doi | 10.1210/en.2014-1433 |
| Citation | Li F, et al. (2015) Conditional deletion of Men1 in the pancreatic beta-cell leads to glucagon-expressing tumor development. Endocrinology 156(1):48-57 |
| abstractText | The tumor suppressor menin is recognized as a key regulator of beta-cell proliferation. To induce tumorigenesis within the pancreatic beta-cells, floxed alleles of Men1 were selectively ablated using Cre-recombinase driven by the insulin promoter. Despite the beta-cell specificity of the RipCre, glucagon-expressing tumors as well as insulinomas developed in old mutant mice. These glucagon-expressing tumor cells were menin deficient and expressed the mature alpha-cell-specific transcription factors Brain-specific homeobox POU domain protein 4 (Brn4) and v-maf musculoaponeurotic fibrosarcoma oncogene family, protein B (MafB). Moreover, the inactivation of beta-cell-specific transcription factors was observed in mutant beta-cells. Our work shows that Men1 ablation in the pancreatic beta-cells leads to the inactivation of specific transcription factors, resulting in glucagon-expressing tumor development, which sheds light on the mechanisms of islet tumorigenesis. |
