Notch and BCR signaling synergistically promote the proliferation of Raji B-lymphoma cells
| Autor: | Li Wang, Ying-Min Liang, Yao-Chun Wang, Hua Han, Guohui Li, Si-Yong Huang, Ping Zhang, Fei He, Dan-Dan Yin, Xing-Bin Hu |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Cancer Research
Cell signaling Lymphoma B-Cell Base Sequence Receptors Notch Reverse Transcriptase Polymerase Chain Reaction B-cell receptor Notch signaling pathway Hematology Biology Cell biology Raji cell Oncology Hes3 signaling axis Cell Line Tumor hemic and lymphatic diseases Proto-Oncogene Proteins c-bcr Humans Cyclin-dependent kinase 8 Electrophoresis Polyacrylamide Gel HES1 Autocrine signalling Cell Proliferation DNA Primers Signal Transduction |
| Zdroj: | Leukemia Research. 33:798-802 |
| ISSN: | 0145-2126 |
| DOI: | 10.1016/j.leukres.2008.09.016 |
| Popis: | The evolutionarily conserved Notch signaling pathway plays a pivotal role in cell proliferation, apoptosis, and cell fate decision from invertebrates to vertebrates, and is oncogenic in some human hematopoietic malignancies. To study the role of Notch signaling in B-lymphoma, we expressed a soluble fragment of human Delta-like1 (hDll1) in E. coli, which was shown to activate the Notch signaling. Incubation of Burkitt's lymphoma Raji cells with the soluble hDll1 led to gamma-secretase-dependent up-regulation of a Notch downstream gene, Hes1. This treatment synergized with B-cell receptor (BCR)-mediated signaling to promote proliferation of Raji cells in vitro, which was cancelled by GSI. We further showed that Notch signaling significantly repressed, while gamma-secretase inhibitor (GSI) enhanced, "natural" apoptosis of Raji cells. Because c-myc is a downstream gene of both Notch signaling and BCR signaling, and GSI blocked c-myc expression in the presence of hDll1 and anti-IgM, Notch signaling might interact with BCR signaling at the level of c-myc expression to regulate proliferation and apoptosis of B-lymphoma cells. |
| Databáze: | OpenAIRE |
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