| Literature DB >> 26832406 |
David M Wong1, Lingli Li2, Sabine Jurado1, Ashleigh King2, Rebecca Bamford1, Meaghan Wall3, Mannu K Walia1, Gemma L Kelly4, Carl R Walkley2, David M Tarlinton4, Andreas Strasser4, Jörg Heierhorst5.
Abstract
How MYC promotes the development of cancer remains to be fully understood. Here, we report that the Zn(2+)-finger transcription factor ASCIZ (ATMIN, ZNF822) synergizes with MYC to activate the expression of dynein light chain (DYNLL1, LC8) in the murine Eμ-Myc model of lymphoma. Deletion of Asciz or Dynll1 prevented the abnormal expansion of pre-B cells in pre-cancerous Eμ-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 Eμ-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.Entities:
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Year: 2016 PMID： 26832406 DOI： 10.1016/j.celrep.2016.01.012
Source DB: PubMed Journal: Cell Rep Impact factor: 9.423