Abstract
Abstract
Background: Diffuse large B-cell lymphoma (DLBCL) is a highly common malignant and heterogeneous non-Hodgkin lymphoma (NHL). Tumor-associated macrophages, predominantly the M2-type, promote tumorigenesis and tumor resistance. Clinical outcome of patients with high neuron-specific enolase (NSE) expression was poorer than that of patients with low NSE level. NSE in tumor-promoting mechanism is currently unclear.
Methods: We explored the role of NSE in macrophages polarization associated with DLBCL immune microenvironment.
Results: We demonstrated that overexpression of NSE in co-cultured lymphoma cells and THP1 cells could promote M2-type polarization and increase P50 nuclear translocation and reduce p65 nuclear translocation, thus inhibiting NF-κB function by increasing p50/p50 homodimer. Moreover, overexpression of NSE in vivo promoted the proliferation of tumor. However, NSE knockdown significantly reduced the tumor volume. Overexpression NSE promoted macrophage towards M2-type polarization.
Conclusion: Our results illustrated that NSE plays a pivotal role in promoting M2 differentiation and reversing M1 to M2 polarization, thereby contributing to lymphoma proliferation and progression.
No relevant conflicts of interest to declare.
