期刊
PLOS ONE
卷 16, 期 7, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0254184
关键词
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资金
- Institut Curie
- Institut National de la Sante et de la Recherche Medicale (INSERM)
- Ligue contre le Cancer
- University Paris-Diderot
- Ligue Nationale Contre le Cancer
- Fondation ARC pour la recherche contre le cancer
- Centre National de la Recherche Scientifique (CNRS)
NFAT transcription factors play crucial roles in T-ALL, essential for the development of leukemia cells. Nfat genes show functional redundancy in T-ALL and may serve as future candidate targets for therapy.
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.
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