The transcription factor ASCIZ and its target DYNLL1 are essential for the development and expansion of MYC-driven B Cell lymphoma
Publication Year 2016-02, Volume 14, Issue #6, Page 1488-99
Journal Title
Cell Rep
Publication Type
Journal Article
How MYC promotes the development of cancer remains to be fully understood. Here, we report that the Zn2+-finger transcription factor ASCIZ (ATMIN, ZNF822) synergizes with MYC to activate the expression of dynein light chain (DYNLL1, LC8) in the murine Emu-Myc model of lymphoma. Deletion of Asciz or Dynll1 prevented the abnormal expansion of pre-B cells in pre-cancerous Emu-Myc mice and potentiated the pro-apoptotic activity of MYC in pre-leukemic immature B cells. Constitutive loss of Asciz or Dynll1 delayed lymphoma development in Emu-Myc mice, and induced deletion of Asciz in established lymphomas extended the survival of tumor-bearing mice. We propose that ASCIZ-dependent upregulation of DYNLL1 levels is essential for the development and expansion of MYC-driven lymphomas by enabling the survival of pre-neoplastic and malignant cells.
Cell Press
WEHI Research Division(s)
Molecular Genetics Of Cancer; Immunology
PubMed ID
NHMRC Grants
NHMRC/1054925 NHMRC/1016701 NHMRC/1086291
Rights Notice
Refer to copyright notice on published article.

Creation Date: 2016-03-14 03:05:32
Last Modified: 2016-05-09 12:23:36
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