TIMP1 induces CD44 expression and the activation and nuclear translocation of SHP1 during the late centrocyte/post-germinal center B cell differentiation
- Authors
- Kim, Young-Sik; Seo, Dong-Wan; Kong, Su-Kang; Lee, Ju-Han; Lee, Eung-Seok; Stetler-Stevenson, Maryalice; Stetler-Stevenson, William G.
- Issue Date
- 28-9월-2008
- Publisher
- ELSEVIER IRELAND LTD
- Keywords
- TIMP1; CD44; SHP1; Hodgkin lymphoma
- Citation
- CANCER LETTERS, v.269, no.1, pp.37 - 45
- Indexed
- SCIE
SCOPUS
- Journal Title
- CANCER LETTERS
- Volume
- 269
- Number
- 1
- Start Page
- 37
- End Page
- 45
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/122694
- DOI
- 10.1016/j.canlet.2008.04.020
- ISSN
- 0304-3835
- Abstract
- Tissue inhibitor of metalloproteinase-1 (TIMP1) is a survival factor of germinal center (GC) B cells, and its over-expression is correlated with aggressive B cell lymphomas and classical Hodgkin lymphomas. We previously demonstrated that TIMP1 down-regulates B-cell receptor and BCL6, and activates interleukins-6,-10 (ILs)/signal transducer and activator of transcription-3 (STAT3) signaling in GC B cells. The activation of ILs/STAT3 signaling can amplify CD44 function, and vice versa, and induce protein-tyrosine phosphatase SHP1 activity by a negative feedback mechanism. Here, we show that TIMP1 up-regulates cell surface CD44 (standard and variants 3 and 7-10) and induces the activity and nuclear localization of SHP1 in an Epstein Barr virus (EBV)-negative Burkitt lymphoma cell line, the neoplastic counterpart of GC centroblasts. These results suggest that TIMP1 functions as a differentiating and survival factor of GC B cells by modulating CD44 and SHP1 in the late centrocyte/post-GC stage, regardless of EBV infection. (C) 2008 Elsevier Ireland Ltd. All rights reserved.
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Collections - Graduate School > Department of Biomedical Sciences > 1. Journal Articles
- College of Medicine > Department of Medical Science > 1. Journal Articles
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