Effect of CXCL12/CXCR4/MMP-2 signaling pathway on biological behavior in triple negative breast cancer / 临床与实验病理学杂志
Chinese Journal of Clinical and Experimental Pathology
; (12): 1203-1208, 2017.
Article
em Zh
| WPRIM
| ID: wpr-695033
Biblioteca responsável:
WPRO
ABSTRACT
Purpose To investigate the effect of CXCL12/CXCR4 and MMP-2 on the biological behavior of triple-negative breast cancer.Method CXCR4-siRNA and pcDNA3.1-CXCR4were transient transfected of in MDA-MB-231 cell line by liposome,RNA and protein were extracted.The mRNA and protein expressions of CXCR4,CXCL12 and MMP-2 were detected by RT-PCR and Western blot respectively.And the migration and proliferation of the transfected cells were detected by Wound-healing assay and MTF assay.Result The experiment of RT-PCR and Westen blot demonstrated that CXCR4 mRNA and protein level expression declines after the expression CXCR4 was down-regulated (P < 0.01),CXCL12 mRNA and protein level expression increased and MMP-2 mRNA and protein level expression increased after the expression CXCR4 was down-regulated (P<0.01),MTT assay and Wound-healing assay results showed that the proliferation ability of 72 h cells was decreased,and the wound healing was slow.The experiment of RT-PCR and Westen blot demonstrated that CXCR4 mRNA and protein level expression increased after the expression CXCR4 was up-regulated (P <0.01).The CXCL12 mRNA and protein level expression declined and MMP-2 mRNA and protein level expression increased after the expression CXCR4 was up-regulated (P <0.01),MTT assay and wound-healing assay results showed that the proliferation ability of 72 h cells was increased,and the wound healing was accelerated.Conclusion CXCL12/CXCR4/ MMP-2 signaling pathway is activated in the triple-negative breast cancer MDA-MB-231 cells,and the inhibition of CXCR4 can reverse the proliferation and migration of malignant biological process.
Texto completo:
1
Índice:
WPRIM
Idioma:
Zh
Revista:
Chinese Journal of Clinical and Experimental Pathology
Ano de publicação:
2017
Tipo de documento:
Article