Clonorchis sinensis excretory–secretory products regulate migration and invasion in cholangiocarcinoma cells via extracellular signal-regulated kinase 1/2/nuclear factor-κB-dependent matrix metalloproteinase-9 expression

2017 ◽  
Vol 47 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Jhang Ho Pak ◽  
Jimin Shin ◽  
In-Sung Song ◽  
Sungbo Shim ◽  
Sung-Wuk Jang
Keyword(s):  
Matrix Metalloproteinase ◽  
Clonorchis Sinensis ◽  
Nuclear Factor Κb ◽  
Matrix Metalloproteinase 9 ◽  
Migration And Invasion ◽  
Nuclear Factor ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Secretory Products ◽  
Metalloproteinase 9

scholarly journals Matrix metalloproteinase-9 is up-regulated by CCL21/CCR7 interaction via extracellular signal-regulated kinase-1/2 signaling and is involved in CCL21-driven B-cell chronic lymphocytic leukemia cell invasion and migration

Blood ◽  
2008 ◽  
Vol 111 (1) ◽  
pp. 383-386 ◽  
Author(s):  
Javier Redondo-Muñoz ◽  
María José Terol ◽  
José A. García-Marco ◽  
Angeles García-Pardo
Keyword(s):  
Chronic Lymphocytic Leukemia ◽  
Matrix Metalloproteinase ◽  
B Cell ◽  
Leukemia Cell ◽  
Matrix Metalloproteinase 9 ◽  
Lymphocytic Leukemia ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Metalloproteinase 9 ◽  
Cell Chronic Lymphocytic Leukemia

B-cell chronic lymphocytic leukemia (B-CLL) progression is frequently accompanied by clinical lymphadenopathy, and the CCL21 chemokine may play an important role in this process. Indeed, CCR7 (the CCL21 receptor), as well as matrix metalloproteinase-9 (MMP-9), are overexpressed in infiltrating B-CLL cells. We have studied whether MMP-9 is regulated by CCL21 and participates in CCL21-dependent migration. CCL21 significantly increased B-CLL MMP-9 production, measured by gelatin zymography. This was inhibited by blocking extracellular signal-regulated kinase-1/2 (ERK1/2) activity or by cell transfection with CCR7-siRNA. Accordingly, CCL21/CCR7 interaction activated the ERK1/2/c-Fos pathway and increased MMP-9 mRNA. CCL21-driven B-CLL cell migration through Matrigel or human umbilical vein endothelial cells (HUVEC) was blocked by anti-CCR7 antibodies, CCR7-siRNA transfection, or the ERK1/2 inhibitor U0126, as well as by anti-MMP-9 antibodies or tissue inhibitor of metalloproteinase 1 (TIMP-1). These results strongly suggest that MMP-9 is involved in B-CLL nodal infiltration and expand the roles of MMP-9 and CCR7 in B-CLL progression. Both molecules could thus constitute therapeutic targets for this disease.

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