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JunB Induced by Constitutive CD30–Extracellular Signal-Regulated Kinase 1/2 Mitogen-Activated Protein Kinase Signaling Activates the CD30 Promoter in Anaplastic Large Cell Lymphoma and Reed-Sternberg Cells of Hodgkin Lymphoma

¹ Fourth Department of Internal Medicine, School of Medicine, Kitasato University; ² Department of Applied Chemistry, Faculty of Science and Technology, Keio University, Kanagawa; ³ Department of Pathology, School of Medicine, Toho University; ⁴ Laboratory of Tumor Cell Biology, Department of Medical Genome Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Tokyo, Japan; ⁵ Department of Pathology, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, Massachusetts; and ⁶ Biochemistry and Molecular Biology, School of Biomedical and Chemical Sciences, University of Western Australia, Crawley, Western Australia, Australia

Requests for reprints: Ryouichi Horie, Fourth Department of Internal Medicine, School of Medicine, Kitasato University, 1-15-1 Sagamihara, Kanagawa 228-8555, Japan. Phone: 81-42-778-8111; Fax: 81-42-778-8441; E-mail: rhorie{at}med.kitasato-u.ac.jp.

High expression of CD30 and JunB is characteristic of tumor cells in anaplastic large cell lymphoma (ALCL) and Hodgkin lymphoma (HL). Possible interactions of CD30 and JunB were examined in this study. We found that the CD30 promoter in tumor cells of both nucleophosmin (NPM)-anaplastic lymphoma kinase (ALK)–positive and NPM-ALK-negative ALCL and HL is regulated by a constitutively active CD30–extracellular signal-regulated kinase (ERK) 1/2 mitogen-activated protein kinase (MAPK). Phosphorylation of ERK1/2 MAPK was confirmed in nuclei of tumor cells in both ALCL and HL. CD30-ERK1/2 MAPK signals induce JunB expression, which maintains high activity of the CD30 promoter. JunB induction seems to be largely independent of nuclear factor B in ALCL and HL. These results show a common mechanism of CD30 overexpression in ALCL and HL, although the outcome of CD30 signaling differs between NPM-ALK-positive ALCL and NPM-ALK-negative ALCL, cutaneous ALCL, and HL as we recently reported.

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