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The transcription factor ASCIZ and its target DYNLL1 are essential for the development and expansion of MYC-driven B Cell lymphoma


Wong, DM; Li, L; Jurado, S; KING, A; Bamford, R; Wall, M; Walia, MK; Kelly, GL; Walkley, CR; Tarlinton, DM; Strasser, A; Heierhorst, J
2016-02
2016-01-27
Cell Rep
Journal Article
14
6
1488-99
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
Molecular Genetics of Cancer; Immunology
10.1016/j.celrep.2016.01.012
26832406
Refer to article for additional funding acknowledgements
Refer to copyright notice on published article.

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