| First Author | Wan L | Year | 2014 |
| Journal | Cancer Cell | Volume | 26 |
| Issue | 1 | Pages | 92-105 |
| PubMed ID | 24981741 | Mgi Jnum | J:214244 |
| Mgi Id | MGI:5588616 | Doi | 10.1016/j.ccr.2014.04.027 |
| Citation | Wan L, et al. (2014) MTDH-SND1 interaction is crucial for expansion and activity of tumor-initiating cells in diverse oncogene- and carcinogen-induced mammary tumors. Cancer Cell 26(1):92-105 |
| abstractText | The Metadherin gene (MTDH) is prevalently amplified in breast cancer and associated with poor prognosis; however, its functional contribution to tumorigenesis is poorly understood. Using mouse models representing different subtypes of breast cancer, we demonstrated that MTDH plays a critical role in mammary tumorigenesis by regulating oncogene-induced expansion and activities of tumor-initiating cells (TICs), whereas it is largely dispensable for normal development. Mechanistically, MTDH supports the survival of mammary epithelial cells under oncogenic/stress conditions by interacting with and stabilizing Staphylococcal nuclease domain-containing 1 (SND1). Silencing MTDH or SND1 individually or disrupting their interaction compromises tumorigenenic potential of TICs in vivo. This functional significance of MTDH-SND1 interaction is further supported by clinical analysis of human breast cancer samples. |
