Contributions
Abstract: EP878
Type: E-Poster Presentation
Session title: Lymphoma Biology & Translational Research
Background
Diffuse large B cell lymphoma (DLBCL) incidence rates have increased year by year, a part of them have poor clinical outcomes, but the underlying mechanism involved is still unclear. Chemokines have been thought to play an important role in occurrence and development of tumors, but they are poorly studied in DLBCL. CC-Chemokine Ligand 2 (CCL2), the most representative of the CC chemokine family members, through binding to its high affinity receptor, CC chemokine receptor 2 (CCR2), has be regarded to involve in tumor growth, angiogenesis, epithelial mesenchymal transition, metastasis and immune escape etc. in recent years, but the role and mechanism in DLBCL has not been reported yet. Our preliminary study showed high expression of CCL2 or CCR2 was correlated with clinicopathological characteristics, and an adverse prognostic factor for overall survival (OS) and progression-free survival (PFS) of DLBCL patients.
Aims
The purpose of this study is to investigate the role of CCL2-CCR2 axis signaling in DLBCL by in vitro experiment.
Methods
CCL2 and CCR2 expression were analyzed in human DLBCL cell lines and normal B lymphocytes by Western blot (WB) and qPCR. CCL2 and CCR2 genes were silenced by lentivirus infection. The proliferation, migration, apoptosis and signaling pathway were detected by CCK8, transwell, flow cytometry (FC) and WB, respectively.
Results
CCL2 and CCR2 were expressed in all human DLBCL cell lines (SUDHL-2, SUDHL-4, SUDHL-6, OCI-Ly8 and OCI-Ly10). Blockade of CCL2-CCR2 axis signaling with lentivirus infection, CCL2 neutralizing antibody or CCR2 antagonist inhibited tumor cell proliferation, migration and anti-apoptosis ability. The CCL2-CCR2 axis involved in the proliferation and migration of DLBCL cells by activating PI3K/Akt signaling pathway, and induced apoptosis through activation of P38MARK signaling pathway.
Conclusion
Our study demonstrates that CCL2/CCR2 axis signaling plays an important role in the development of DLBCL by stimulating cell proliferation, migration and anti-apoptosis. The inhibition of CCL2 or CCR2 may, therefore, be a potential target for anticancer therapy in DLBCL.
Keyword(s):
Abstract: EP878
Type: E-Poster Presentation
Session title: Lymphoma Biology & Translational Research
Background
Diffuse large B cell lymphoma (DLBCL) incidence rates have increased year by year, a part of them have poor clinical outcomes, but the underlying mechanism involved is still unclear. Chemokines have been thought to play an important role in occurrence and development of tumors, but they are poorly studied in DLBCL. CC-Chemokine Ligand 2 (CCL2), the most representative of the CC chemokine family members, through binding to its high affinity receptor, CC chemokine receptor 2 (CCR2), has be regarded to involve in tumor growth, angiogenesis, epithelial mesenchymal transition, metastasis and immune escape etc. in recent years, but the role and mechanism in DLBCL has not been reported yet. Our preliminary study showed high expression of CCL2 or CCR2 was correlated with clinicopathological characteristics, and an adverse prognostic factor for overall survival (OS) and progression-free survival (PFS) of DLBCL patients.
Aims
The purpose of this study is to investigate the role of CCL2-CCR2 axis signaling in DLBCL by in vitro experiment.
Methods
CCL2 and CCR2 expression were analyzed in human DLBCL cell lines and normal B lymphocytes by Western blot (WB) and qPCR. CCL2 and CCR2 genes were silenced by lentivirus infection. The proliferation, migration, apoptosis and signaling pathway were detected by CCK8, transwell, flow cytometry (FC) and WB, respectively.
Results
CCL2 and CCR2 were expressed in all human DLBCL cell lines (SUDHL-2, SUDHL-4, SUDHL-6, OCI-Ly8 and OCI-Ly10). Blockade of CCL2-CCR2 axis signaling with lentivirus infection, CCL2 neutralizing antibody or CCR2 antagonist inhibited tumor cell proliferation, migration and anti-apoptosis ability. The CCL2-CCR2 axis involved in the proliferation and migration of DLBCL cells by activating PI3K/Akt signaling pathway, and induced apoptosis through activation of P38MARK signaling pathway.
Conclusion
Our study demonstrates that CCL2/CCR2 axis signaling plays an important role in the development of DLBCL by stimulating cell proliferation, migration and anti-apoptosis. The inhibition of CCL2 or CCR2 may, therefore, be a potential target for anticancer therapy in DLBCL.
Keyword(s):