CCL2‐CCR2 AXIS SIGNALING PROMOTES DIFFUSE LARGE B‐CELL LYMPHOMA CELL SURVIVAL AND INVASION

Objective: Diffuse large B cell lymphoma (DLBCL) incidence rates have increased year by year, a part of them poor clinical outcomes, but the underlying mechanism involved is still unclear. Chemokines been thought to play an important role in occurrence and development tumors, they are poorly studied DLBCL. CC-Chemokine Ligand 2 (CCL2), most representative CC chemokine family members, through binding its high affinity receptor, receptor (CCR2), has be regarded involve tumor growth, angiogenesis, epithelial mesenchymal transition, metastasis immune escape etc. recent years, DLBCL not reported yet. Our preliminary study showed expression CCL2 or CCR2 was correlated with clinicopathological characteristics, adverse prognostic factor for overall survival (OS) progression-free (PFS) patients. The purpose this investigate CCL2-CCR2 axis signaling vitro experiment. Methods: were analyzed human lines normal lymphocytes Western blot (WB) qPCR. genes silenced lentivirus infection. proliferation, migration, apoptosis pathway detected CCK8, transwell, flow cytometry (FC) WB, respectively. Results: expressed all (SUDHL-2, SUDHL-4, SUDHL-6, OCI-Ly8 OCI-Ly10). Blockade infection, neutralizing antibody antagonist inhibited migration anti-apoptosis ability. proliferation cells activating PI3K/Akt pathway, induced activation P38MARK pathway. Conclusions: demonstrates that CCL2/CCR2 plays stimulating anti-apoptosis. inhibition may, therefore, potential target anticancer therapy Keywords: Aggressive B-cell non-Hodgkin No conflicts interests pertinent abstract.