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Despite the recognition that these genetic lesions cooperate in leukemogenesis, there have been no mechanistic studies addressing how <jats:italic>TLX1<\/jats:italic> and <jats:italic>NOTCH1<\/jats:italic> functionally interact to promote the leukemic phenotype.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>Global gene expression profiling after downregulation of TLX1 and inhibition of the NOTCH pathway in ALL-SIL cells revealed that TLX1 synergistically regulated more than 60% of the NOTCH-responsive genes. Structure-function analysis demonstrated that TLX1 binding to Groucho-related TLE corepressors was necessary for maximal transcriptional regulation of the NOTCH-responsive genes tested, implicating TLX1 modulation of the NOTCH-TLE regulatory network. Comparison of the dataset to publicly available biological databases indicated that the TLX1\/NOTCH-coregulated genes are frequently targeted by MYC. Gain- and loss-of-function experiments confirmed that MYC was an essential mediator of TLX1\/NOTCH transcriptional output and growth promotion in ALL-SIL cells, with TLX1 contributing to the NOTCH-MYC regulatory axis by posttranscriptional enhancement of MYC protein levels. Functional classification of the TLX1\/NOTCH-coregulated targets also showed enrichment for genes associated with other human cancers as well as those involved in developmental processes. In particular, we found that TLX1, NOTCH and MYC coregulate <jats:italic>CD1B<\/jats:italic> and <jats:italic>RAG1<\/jats:italic>, characteristic markers of early cortical thymocytes, and that concerted downregulation of the TLX1 and NOTCH pathways resulted in their irreversible repression.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions<\/jats:title>\n            <jats:p>We found that TLX1 and NOTCH synergistically regulate transcription in T-ALL, at least in part via the sharing of a TLE corepressor and by augmenting expression of MYC. We conclude that the TLX1\/NOTCH\/MYC network is a central determinant promoting the growth and survival of TLX1<jats:sup>+<\/jats:sup> T-ALL cells. In addition, the TLX1\/NOTCH\/MYC transcriptional network coregulates genes involved in T cell development, such as CD1 and RAG family members, and therefore may prescribe the early cortical stage of differentiation arrest characteristic of the TLX1 subgroup of T-ALL.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/1476-4598-9-181","type":"journal-article","created":{"date-parts":[[2010,7,12]],"date-time":"2010-07-12T01:24:54Z","timestamp":1278897894000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["TLX1 and NOTCH coregulate transcription in T cell acute lymphoblastic leukemia cells"],"prefix":"10.1186","volume":"9","author":[{"given":"Irene","family":"Riz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teresa S","family":"Hawley","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Truong V","family":"Luu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Norman H","family":"Lee","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert G","family":"Hawley","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2010,7,9]]},"reference":[{"key":"696_CR1","doi-asserted-by":"publisher","first-page":"381","DOI":"10.1242\/dev.02746","volume":"134","author":"SD Hueber","year":"2007","unstructured":"Hueber SD, Bezdan D, Henz SR, Blank M, Wu H, Lohmann I: Comparative analysis of Hox downstream genes in Drosophila. 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