Altered Expressions of CD30, c-Jun N-Terminal Kinase, NF-κB and JunB Are Involved in Disease Progression in CD30-Positive Anaplastic Large Cell Lymphoma
Autor: | Takashi Maeda, Hidetoshi Nakashima, Tsuyoshi Nakamaki, Shigeru Tomoyasu, Masamichi Hattori, Takako Usui, Kunihiko Fukuchi |
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Rok vydání: | 2005 |
Předmět: | |
Zdroj: | Blood. 106:2827-2827 |
ISSN: | 1528-0020 0006-4971 |
DOI: | 10.1182/blood.v106.11.2827.2827 |
Popis: | Anaplastic large cell lymphoma kinase (ALK)-negative anaplastic large cell lymphoma (ALCL) is an aggressive T cell lymphoma. CD30 is a characteristic cell surface protein overexpressed in ALCL cells as well as in malignant cells of Hodgkin lymphoma. CD30-mediated signals are molecular target(s) in the therapy for CD30-positive lymphoma. We studied molecular pathway(s) involved in the disease progression in two ALK- negative CD30-positive ALCL cell lines (N1, N2), which are recently established. In vitro culture, N1 and N2 represent early and advanced stage lymphoma phenotype, respectively. N2, compared to N1, was characterized by the increase of colony formation in soft agar more than 100 fold, the increase of cell surface expression of CD30 protein (p Taken together, the present study showed that aberrantly activated JNK/AP-1 and NF- κB, at least in part, are responsible for disease progression in some types of CD30-positive ALCL, although details of signaling pathways triggered by altered CD30 in ALCL cells still remained to be elucidated. In addition, the data suggested that JunB, as a downstream molecule regulated by JNK and/or NF- κB, had a putative tumor suppressor function in CD30-positive lymphoma cells. |
Databáze: | OpenAIRE |
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