Carcinogenesis, Teratogenesis & Mutagenesis ›› 2008, Vol. 20 ›› Issue (2): 89-092.doi: 10.3969/j.issn.1004-616x.2008.02.003

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Inhibitory Effect of Polypeptide on CXCR4-related Metastasis of Breast Cancer Cell Line

YANG Qing-ling1, LI Cheng-hua2, DING Yong-xing2, CHEN Chang-jie1, ZHANG Ju1, WANG Hui1   

  1. 1.Department of Biochemistry ＆ Molecular Biology, Bengbu Medical College, Bengbu 233000, Anhui; 2. Oncology Department of the Central Hospital of Bengbu, Bengbu 233000, Anhui,China
  • Received:2007-04-29 Revised:2007-09-06 Online:2008-03-30 Published:2008-03-30

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Abstract: BACKGROUND AND AIM: CXCR4-stromal cell-derived factor-1(CXCR4- SDF-1α) system has been proved to be involved in targeting metastasis of breast cancer. Some antagonists of CXCR4 have shown inhibitory effects on breast cancer metastasis. This study was to investigate the inhibitory effect of N-terminal 21-mer peptide(NT21MP) on CXCR4-related metastasis of breast cancer cell line MCF-7. MATERIALS AND METHODS: The suppressed expression of CXCR4 protein was examined by immunocytochemistry and fluorescent antibody on MCF-7 and SK-BR3. Adhesion and chemotaxis assays were used to evaluate the effect of NT21MP on MCF-7 cells in different stages of metastasis. Clone formation rate was assessed by agar clone assay. RESULTS: The expression of CXCR4 was markedly decreased by NT21MP (0.1,0.5,1.0,4.0 μg/ml) compared with negative control after 24 h. Inhibition of cell adherence to fibronectin(FN) and Matrigel in a concentration-dependent manner was found after treatment with NT21MP (5,50,100,500 ng/ml)(P<0.05). The number of migration in the presence of NT21MP was lower than that of control (P<0.05). Peptide suppressed colony formation of MCF-7 cells in a concentration-dependent manner and inhibitive ratio was from 22.0％ to 51.8％. CONCLUSION: NT21MP could decrease expression of CXCR4. Adhesion to FN and Matrigel, chemotactic activity toward chemokine SDF-1α, and clone formation rate of MCF-7 cell were all suppressed.

Key words: CXCR4, N-terminal 21-mer peptide, breast cancer, metastasis