hIgD promotes human Burkitt lymphoma Daudi cell proliferation by accelerated G1/S transition via IgD receptor activity.

Abstract	The aim of the present study was to investigate the role and molecular mechanism of human IgD (hIgD) on the proliferation of human Burkitt lymphoma Daudi cells in vitro. Logarithmically growing Daudi cells were treated with hIgD for different time periods, and cell proliferation was evaluated by cell counting kit-8 (CCK-8) assay. The expressions of Daudi surface markers and IgD receptor (IgDR) as well as cell cycle and apoptosis were measured by flow cytometry analysis. Our results showed that hIgD stimulation induced proliferation and IgDR expression and reduced the apoptosis of Daudi cells. Treatment with hIgD promoted progression of the cell cycle at the G1/S transition, and this was accompanied by upregulation of c-myc, cyclin D3, and CDK6 as well as downregulation of p16 mRNA and protein levels. Moreover, hIgD treatment also upregulated the expression of tyrosine phosphorylation of 70 kDa protein (IgDR) and p-Lyn. Taken together, these results indicate that hIgD can induce Daudi cell proliferation through activating IgDR to initiate the tyrosine phosphorylation signaling cascade to accelerate the G1/S transition.
Authors	Xing Dai, YuJing Wu, XiaoYi Jia, Yan Chang, HuaXun Wu, Chun Wang, HengShi Chen, WenSheng Chen, Qiong Huang, Wei Wei
Journal	Immunologic research (Immunol Res) Vol. 64 Issue 4 Pg. 978-87 (08 2016) ISSN: 1559-0755 [Electronic] United States
PMID	26724941 (Publication Type: Journal Article)
Chemical References	CDKN2A protein, human Cyclin D3 Cyclin-Dependent Kinase Inhibitor p16 Immunoglobulin D MYC protein, human Proto-Oncogene Proteins c-myc Receptors, Fc immunoglobulin D receptor CDK6 protein, human Cyclin-Dependent Kinase 6
Topics	Burkitt Lymphoma (immunology, pathology, therapy) Cell Line, Tumor Cell Proliferation Cyclin D3 (metabolism) Cyclin-Dependent Kinase 6 (metabolism) Cyclin-Dependent Kinase Inhibitor p16 (genetics, metabolism) G1 Phase Cell Cycle Checkpoints Gene Expression Regulation, Neoplastic Humans Immunoglobulin D (metabolism) Immunotherapy (methods) Molecular Targeted Therapy Phosphorylation Proto-Oncogene Proteins c-myc (metabolism) Receptors, Fc (metabolism) Signal Transduction

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