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Sensitisation of c-MYC-induced B-lymphoma cells to apoptosis by ATF2

J Walczynski1, S Lyons1, N Jones1

  • 1Department of Cell Regulation, Paterson Institute for Cancer Research, University of Manchester, Manchester, UK.

Oncogene
|February 19, 2013
PubMed

Insights

Transcription factors ATF2 and ATF7 are crucial in preventing lymphoma. Their absence accelerates Eμ-Myc-induced lymphoma and reduces apoptosis, highlighting their role in B-cell cancer.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Transcription factors activating transcription factor 2 (ATF2) and ATF7 are homologous AP-1 family members.
  • Their function requires phosphorylation by mitogen-activated protein (MAP) kinases and is stimulated by growth factors and stress.

Purpose of the Study:

  • To investigate the role of ATF2 and ATF7 in B-cell lymphomas.
  • To determine the impact of ATF2 and ATF7 on lymphoma development and apoptosis in response to oncogenic transformation.

Main Methods:

  • Analysis of ATF2 and c-Jun N-terminal kinase (JNK) expression in human and mouse B-cell lymphomas.
  • B cell-specific deletion of ATF2 and ATF7 in a mouse model of Eμ-Myc-induced lymphoma.
  • Assessment of apoptosis in lymphoma cells with and without ATF2/7.

Main Results:

  • ATF2 and JNK are significantly up-regulated in B-cell lymphomas.
  • Deletion of ATF2 and ATF7 accelerates Eμ-Myc-induced lymphoma onset in mice.
  • Loss of ATF2/7 desensitizes lymphoma cells to apoptosis, both spontaneous and stress-induced.

Conclusions:

  • c-MYC oncogenic transformation induces stress-mediated activation of ATF2 and ATF7.
  • ATF2 and ATF7 act as critical regulators of apoptosis in B-cell lymphomas.
  • These transcription factors play a protective role against lymphoma development.

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