B Wu1, F Zhang, M Yu, P Zhao, W Ji, H Zhang, J Han, R Niu. 1. Key Laboratory of Breast Cancer Prevention and Therapy, Ministry of Education, Tianjin Medical University Cancer Institute and Hospital, Tianjin Medical University, Tianjin, China.
Abstract
OBJECTIVE: The metastatic ability of breast cancer cells with chemoresistant properties is higher when compared to that of their parental wild-type cells. Expression of AnnexinA2 (Anxa2), a 36-kDa calcium-dependent phospholipid binding protein, is increased in metastatic tumours and has been found to be associated with the phenotype of drug resistance and metastasis. MATERIALS AND METHODS AND RESULTS: In the present study, we found that up-regulation of Anxa2 correlates with enhanced migration and invasion ability of MCF-7 breast cancer cells both in vitro and in vivo. Western blot analysis revealed that exposure to chemotherapeutic drugs may induce elevated expression of Anxa2. In addition, our data have shown that Anxa2 might influence proliferation, migration and invasion of MCF-7 cells by increasing expression of c-myc and cyclin D1 via activation of Erk1/2 signalling pathways. CONCLUSION: Our findings suggest that up-regulation of Anxa2 may play an important role in modulating proliferation and invasion of breast cancer MCF-7 cells through regulation of many relevant downstream target genes.
OBJECTIVE: The metastatic ability of breast cancer cells with chemoresistant properties is higher when compared to that of their parental wild-type cells. Expression of AnnexinA2 (Anxa2), a 36-kDa calcium-dependent phospholipid binding protein, is increased in metastatic tumours and has been found to be associated with the phenotype of drug resistance and metastasis. MATERIALS AND METHODS AND RESULTS: In the present study, we found that up-regulation of Anxa2 correlates with enhanced migration and invasion ability of MCF-7 breast cancer cells both in vitro and in vivo. Western blot analysis revealed that exposure to chemotherapeutic drugs may induce elevated expression of Anxa2. In addition, our data have shown that Anxa2 might influence proliferation, migration and invasion of MCF-7 cells by increasing expression of c-myc and cyclin D1 via activation of Erk1/2 signalling pathways. CONCLUSION: Our findings suggest that up-regulation of Anxa2 may play an important role in modulating proliferation and invasion of breast cancer MCF-7 cells through regulation of many relevant downstream target genes.
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