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Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B

Official URL:http://www.ncbi.nlm.nih.gov/pmc/articles/PMC126136/
PubMed:View item in PubMed
Creators Name:Mathas, S. and Hinz, M. and Anagnostopoulos, L. and Krappmann, D. and Lietz, A. and Jundt, F. and Bommert, K. and Mechta-Grigoriou, F. and Stein, H. and Doerken, B. and Scheidereit, C.
Journal Title:EMBO Journal
Journal Abbreviation:EMBO J
Volume:21
Number:15
Page Range:4104-4113
Date:1 August 2002
Keywords:Lymphoma, MAPK, Metastasis, Oncogenesis, Target Genes
Abstract:AP-1 family transcription factors have been implicated in the control of proliferation, apoptosis and malignant transformation. However, their role in oncogenesis is unclear and no recurrent alterations of AP-1 activities have been described in human cancers. Here, we show that constitutively activated AP-1 with robust c-Jun and JunB overexpression is found in all tumor cells of patients with classical Hodgkin's disease. A similar AP-1 activation is present in anaplastic large cell lymphoma (ALCL), but is absent in other lymphoma types. Whereas c-Jun is up-regulated by an autoregulatory process, JunB is under control of NF-kappa B. Activated AP-1 supports proliferation of Hodgkin cells, while it suppresses apoptosis of ALCL cells. Furthermore, AP-1 cooperates with NF-kappa B and stimulates expression of the cell-cycle regulator cyclin D2, proto-oncogene c-met and the lymphocyte homing receptor CCR7, which are all strongly expressed in primary HRS cells. Together, these data suggest an important role of AP-1 in lymphoma pathogenesis.
ISSN:0261-4189
Publisher:Nature Publishing Group (U.S.A.)
Item Type:Article

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