The Transcription Factor ASCIZ and Its Target DYNLL1 Are Essential for the Development and Expansion of MYC-Driven B Cell Lymphoma | Zendy

David M. Wong | Zendy; Lingli Li | Zendy; Sabine Jurado | Zendy; Ashleigh King | Zendy; Rebecca Bamford | Zendy; Meaghan Wall | Zendy; Mannu Walia | Zendy; Gemma L. Kelly | Zendy; Carl R. Walkley | Zendy; David M. Tarlinton | Zendy; Andreas Strasser | Zendy; Jörg Heierhorst | Zendy

Open Access

The Transcription Factor ASCIZ and Its Target DYNLL1 Are Essential for the Development and Expansion of MYC-Driven B Cell Lymphoma

Author(s) -

David M. Wong,

Lingli Li,

Sabine Jurado,

Ashleigh King,

Rebecca Bamford,

Meaghan Wall,

Mannu Walia,

Gemma L. Kelly,

Carl R. Walkley,

David M. Tarlinton,

Andreas Strasser,

Jörg Heierhorst

Publication year - 2016

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2016.01.012

Subject(s) - lymphoma , transcription factor , downregulation and upregulation , cancer research , proto oncogene proteins c myc , chemistry , b cell , microbiology and biotechnology , gene , biology , immunology , antibody , biochemistry

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.

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