| Breast cancer is the most common cancer in women worldwide,and it put a heavy burden on patients,their families and society.No matter whether it is chemotherapy,immunotherapy,endocrine therapy or more,the best solution has not been found.RYBP as a component of PcG complexes or binding to different transcriptional factor regulate genes expression.It also can promotes or inhibits cell apoptosis by interacting with apoptosis-associated proteins.Several studies have demonstrated aberrant expression of RYBP in various human cancer.It demonstrated that RYBP has a certain relationship with the tumor.In our previous study,RYBP was shown to promote breast cancer cell proliferation,migration,invasion,decrease of chemosensitivity,and maintenance of stem cell characteristics.The above results suggest that RYBP is closely related to breast cancer.Tumors can induce endothelial cells to form new blood vessels,Microvascular formation is one of the necessary conditions for tumor cell invasion and metastasis.To further investigate the regulation and function of RYBP in breast cancer,we can better understand the role of RYBP in the development of breast cancer.We constructed a RYBP knockdown plasmid based on the miR-30 backbone and established a lentiviral knockdown cell line that stably down-regulated the expression of RYBP,including MDA-MB-231/miR-30-shRYBP,MDA-MB-231/shRYBP.The proliferation ability of HUVEC cells co-cultured with tumor cell condition medium was monitored by RTCA real-time unlabeled cell dynamic analyzer.Wound healing assays was used to investgated the impact on HUVEC migration with the above cell condition medium.Matrigel tube formation experiments was be applied to observe angiogenic ability.Aortic ring assay was used to explore angiogenesis in vivo.Our results suggest that down-regulation of RYBP expression in MDA-MB-231 cells can reduce endothelial cell proliferation,adhesion,migration,tube formation and angiogenesis. |
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