| First Author | Sato S | Year | 2016 |
| Journal | Cell Rep | Volume | 16 |
| Issue | 4 | Pages | 917-927 |
| PubMed ID | 27425618 | Mgi Jnum | J:238661 |
| Mgi Id | MGI:5823326 | Doi | 10.1016/j.celrep.2016.06.058 |
| Citation | Sato S, et al. (2016) Mesenchymal Tumors Can Derive from Ng2/Cspg4-Expressing Pericytes with beta-Catenin Modulating the Neoplastic Phenotype. Cell Rep 16(4):917-27 |
| abstractText | The cell of origin for most mesenchymal tumors is unclear. One cell type that contributes to this lineages is the pericyte, a cell expressing Ng2/Cspg4. Using lineage tracing, we demonstrated that bone and soft tissue sarcomas driven by the deletion of the Trp53 tumor suppressor, or desmoid tumors driven by a mutation in Apc, can derive from cells expressing Ng2/Cspg4. Deletion of the Trp53 tumor suppressor gene in these cells resulted in the bone and soft tissue sarcomas that closely resemble human sarcomas, while stabilizing beta-catenin in this same cell type caused desmoid tumors. Comparing expression between Ng2/Cspg4-expressing pericytes lacking Trp53 and sarcomas that arose from deletion of Trp53 showed inhibition of beta-catenin signaling in the sarcomas. Activation of beta-catenin inhibited the formation and growth of sarcomas. Thus, pericytes can be a cell of origin for mesenchymal tumors, and beta-catenin dysregulation plays an important role in the neoplastic phenotype. |
