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| Item Type: | Article |
|---|---|
| Title: | Aberrantly expressed c-Jun and JunB are a hallmark of Hodgkin lymphoma cells, stimulate proliferation and synergize with NF-kappa B |
| Creators: |
Mathas, S.  ORCID: https://orcid.org/0000-0001-9626-1413, Hinz, M. ORCID: https://orcid.org/0000-0003-2611-4121, Anagnostopoulos, L., Krappmann, D. ORCID: https://orcid.org/0000-0001-7640-3234, Lietz, A., Jundt, F., Bommert, K., Mechta-Grigoriou, F., Stein, H., Dörken, B. ORCID: https://orcid.org/0000-0001-7991-3643 and Scheidereit, C. ORCID: https://orcid.org/0000-0002-0446-6129
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| 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. |
| Keywords: | Lymphoma, MAPK, Metastasis, Oncogenesis, Target Genes |
| Source: | EMBO Journal |
| ISSN: | 0261-4189 |
| Publisher: | Oxford University Press |
| Volume: | 21 |
| Number: | 15 |
| Page Range: | 4104-4113 |
| Date: | 1 August 2002 |
| Official Publication: | http://www.ncbi.nlm.nih.gov/pmc/articles/PMC126136/ |
| PubMed: | View item in PubMed |
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