Objective To explore the role of integrin in CCL18 for promoting breast cancer SK-3 rd cells invasion and migration process to illuminate the molecular mechanism of CCL 18 for promoting breast cancer SK-3 rd cells invasion and migration process . Methods The flow cytometry was adopted to detect CCL18-induced integrin aggregation ;Western blot was used to detect the focal adhesion kinase(FAK ) activation ,the infiltrating migrationin experiment was adopted to determine the invasion and migration of SK-3rd cells and the siRNAs transfection was used to detect the expression of silence integrin β1 .Results CCL18 promoted the in-tegrinβ1 aggregation in breast cancer SK-3rd cell surface and further promoted the integrin-mediated phosphorylated activation of FAK .Under the reaction of CCL18 ,the cells number of SK-3rd cellular invasion and migration was increased by ten times (P<0 .01) ,which was obviously decreased by siRNA silenced integrin β1 .Conclusion CCL18 promotes breast cancer invasion and mi-gration via integrin aggregation .

AIM:To investigate the regulation of miR-222 on BCL2L13 gene and its effect on the growth and apoptosis of HBx-HepG2 cells, and to explore the underlying molecular mechanisms .METHODS:The expression level of miR-222 was detected by RT-qPCR.The HBx-HepG2 cell growth was examined by MTT and colony formation assays .The cell cycle and apoptosis were analyzed by flow cytometry .The recombination vector pmirGLO-BCL2L13 was constructed, and dual-luciferase reporter experiment was performed to validate the target of miR-222.RESULTS:The expression level of miR-222 in the HBx-HepG2 cells was significantly higher than that in the L 02 cells ( P<0.05 ) .Over-expression of miR-222 enhanced HBx-HepG2 cell growth, changed cell cycle, and inhibited apoptosis (P<0.05).Knockdown of miR-222 reduced HBx-HepG2 cell growth, changed cell cycle, and increased cell apoptotic rate (P<0.05).BCL2L13 was down-regulated in the HBx-HepG2 cells as compared with L02 cells (P<0.05), and knockdown of miR-222 in the HBx-HepG2 cells increased the expression level of BCL2L13 (P<0.05).The results of dual-luciferase reporter assay and re-store experiment showed that miR-222 negatively regulated the expression of BCL2L13 via targeting 3’ UTR of BCL2L13, resulting in the promotion of HBx-HepG2 cell growth .CONCLUSION: miR-222 enhances HBx-HepG2 cell growth via down-regulation of BCL2L13.