| First Author | Catherinet C | Year | 2021 |
| Journal | PLoS One | Volume | 16 |
| Issue | 7 | Pages | e0254184 |
| PubMed ID | 34234374 | Mgi Jnum | J:326349 |
| Mgi Id | MGI:6726253 | Doi | 10.1371/journal.pone.0254184 |
| Citation | Catherinet C, et al. (2021) NFAT transcription factors are essential and redundant actors for leukemia initiating potential in T-cell acute lymphoblastic leukemia. PLoS One 16(7):e0254184 |
| abstractText | T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive malignancy with few available targeted therapies. We previously reported that the phosphatase calcineurin (Cn) is required for LIC (leukemia Initiating Capacity) potential of T-ALL pointing to Cn as an interesting therapeutic target. Calcineurin inhibitors have however unwanted side effect. NFAT transcription factors play crucial roles downstream of calcineurin during thymocyte development, T cell differentiation, activation and anergy. Here we elucidate NFAT functional relevance in T-ALL. Using murine T-ALL models in which Nfat genes can be inactivated either singly or in combination, we show that NFATs are required for T-ALL LIC potential and essential to survival, proliferation and migration of T-ALL cells. We also demonstrate that Nfat genes are functionally redundant in T-ALL and identified a node of genes commonly deregulated upon Cn or NFAT inactivation, which may serve as future candidate targets for T-ALL. |
