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hIgD promotes human Burkitt lymphoma Daudi cell proliferation by accelerated G1/S transition via IgD receptor
Xing Dai1, YuJing Wu1, XiaoYi Jia1
1Key Laboratory of Anti-inflammatory and Immune Medicine of the Education Ministry of China, Anhui Collaborative Innovation Center of Anti-inflammatory and Immune Medicine, Institute of Clinical Pharmacology, Anhui Medical University, Meishan Road 81, Hefei, 230032, China.
Insights
Human IgD (hIgD) stimulates human Burkitt lymphoma Daudi cell proliferation by activating the IgD receptor (IgDR). This process accelerates the cell cycle and reduces apoptosis, offering insights into lymphoma progression.
Area of Science:
- Immunology
- Molecular Biology
- Cancer Research
Background:
- Human IgD (hIgD) is a crucial immunoglobulin isotype with incompletely understood functions.
- Burkitt lymphoma is an aggressive non-Hodgkin lymphoma with a high proliferation rate.
Purpose of the Study:
- To investigate the role of hIgD in the proliferation of human Burkitt lymphoma Daudi cells.
- To elucidate the molecular mechanisms underlying hIgD-induced cell proliferation.
Main Methods:
- Daudi cells were treated with hIgD and proliferation was assessed using CCK-8 assay.
- Flow cytometry was employed to analyze surface markers, IgD receptor (IgDR) expression, cell cycle, and apoptosis.
- mRNA and protein levels of key cell cycle regulators (c-myc, cyclin D3, CDK6, p16) were measured.
Main Results:
- hIgD stimulation significantly increased Daudi cell proliferation and IgDR expression.
- hIgD treatment reduced apoptosis and promoted cell cycle progression at the G1/S transition.
- Upregulation of c-myc, cyclin D3, CDK6, and tyrosine phosphorylation of IgDR and p-Lyn was observed, alongside p16 downregulation.
Conclusions:
- hIgD induces Daudi cell proliferation by activating IgDR.
- The signaling cascade involves tyrosine phosphorylation and accelerates G1/S transition, suggesting a role in lymphoma pathogenesis.
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.
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