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CD150-mediated Akt signalling pathway in normal and malignant B cells
M Yurchenko1, L M Shlapatska, O L Romanets
1R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology NAS of Ukraine, Kyiv 03022, Ukraine. myurchenko@hotmail.com
Experimental Oncology
|March 23, 2011
Summary
CD150 signaling activates Akt in B cells, influencing survival. This pathway involves PI3K interaction and phosphorylation of key targets like FoxO1 and GSK-3β, crucial for B cell survival.
Area of Science:
- Immunology
- Cell Biology
- Molecular Signaling
Background:
- The CD150 receptor plays a role in immune cell regulation.
- Understanding signaling pathways in B cell malignancies is critical for therapeutic development.
Purpose of the Study:
- To investigate the upstream and downstream signaling events of the CD150-mediated Akt pathway.
- To compare these events in normal human B cells, EBV-transformed lymphoblastoid cells (LCL), and Hodgkin's lymphoma (HL) B cell lines.
Main Methods:
- Utilized immunoprecipitation, Western blot analysis, and surface plasmon resonance (SPR) for protein-protein interactions.
- Employed immunostaining and subcellular fractionation to determine protein localization.
- Assessed protein phosphorylation and expression levels via Western blot.
Main Results:
- CD150 ligation induced Akt activation in normal B cells, LCL, and HL cell lines.
- The p85α subunit of PI3K directly associated with the CD150 cytoplasmic tail, dependent on tyrosine phosphorylation.
- CD150 triggered phosphorylation of FoxO1 in all cell types and GSK-3β in LCL and HL cells.
Conclusions:
- Demonstrated that the CD150 receptor activates the PI3K-Akt signaling pathway in normal, EBV-transformed, and malignant B cells.
- CD150-mediated phosphorylation of Akt targets (GSK-3β, FoxO1) may promote survival and inhibit apoptosis in EBV-transformed and HL cells.
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