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Article

Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines

  • Authors:
    • Dalin Di
    • Lei Chen
    • Lina Wang
    • Ping Sun
    • Yanfei Liu
    • Zhiwei Xu
    • Jiyu Ju
  • View Affiliations / Copyright

    Affiliations: Department of Immunology, Weifang Medical University, Weifang, Shandong 261053, P.R. China, Department of Hematology, Affiliated Hospital of Weifang Medical University, Weifang, Shandong 261053, P.R. China
  • Pages: 1541-1548
    |
    Published online on: January 5, 2016
       https://doi.org/10.3892/or.2016.4543
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Abstract

Intercellular adhesion molecule-1 (ICAM-1) is a cell surface glycoprotein that belongs to immunoglobulin superfamily and plays an important role in tumor cell expansion or metastasis. However, the detailed mechanisms of ICAM-1 in breast cancer remain unclear. In this study, we evaluated the expression level of ICAM-1 in breast cancer using tissue microarray and clinical tissue specimens by immunohistochemical method, and the results revealed that ICAM-1 is highly expressed in the breast cancer tissues. To investigate whether ICAM-1 can affect the metastasis ability in breast cancer, we knocked down ICAM-1 expression in breast cancer cell line MCF-7 by using lentivirus-mediated RNA interference (RNAi). As a result, we stably silenced ICAM-1 expression in MCF-7 cells by infection with lentivirus expressing green fluorescent protein (GFP), the change of metastatic ability of MCF-7 cells was assessed by wound-healing assay, Transwell assay or clone formation assay. Our results showed that silencing of ICAM-1 can inhibit the metastatic ability of MCF-7 cell lines in vitro significantly, and the decreased migration and invasion was accompanied by a reduction of MMP-14. These results implying that ICAM-1 might be involved in the progression of breast cancer metastasis and lentivirus-mediated silencing of ICAM-1 might be a potential therapeutic approach for the treatment of breast cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Di D, Chen L, Wang L, Sun P, Liu Y, Xu Z and Ju J: Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines. Oncol Rep 35: 1541-1548, 2016.
APA
Di, D., Chen, L., Wang, L., Sun, P., Liu, Y., Xu, Z., & Ju, J. (2016). Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines. Oncology Reports, 35, 1541-1548. https://doi.org/10.3892/or.2016.4543
MLA
Di, D., Chen, L., Wang, L., Sun, P., Liu, Y., Xu, Z., Ju, J."Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines". Oncology Reports 35.3 (2016): 1541-1548.
Chicago
Di, D., Chen, L., Wang, L., Sun, P., Liu, Y., Xu, Z., Ju, J."Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines". Oncology Reports 35, no. 3 (2016): 1541-1548. https://doi.org/10.3892/or.2016.4543
Copy and paste a formatted citation
x
Spandidos Publications style
Di D, Chen L, Wang L, Sun P, Liu Y, Xu Z and Ju J: Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines. Oncol Rep 35: 1541-1548, 2016.
APA
Di, D., Chen, L., Wang, L., Sun, P., Liu, Y., Xu, Z., & Ju, J. (2016). Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines. Oncology Reports, 35, 1541-1548. https://doi.org/10.3892/or.2016.4543
MLA
Di, D., Chen, L., Wang, L., Sun, P., Liu, Y., Xu, Z., Ju, J."Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines". Oncology Reports 35.3 (2016): 1541-1548.
Chicago
Di, D., Chen, L., Wang, L., Sun, P., Liu, Y., Xu, Z., Ju, J."Downregulation of human intercellular adhesion molecule-1 attenuates the metastatic ability in human breast cancer cell lines". Oncology Reports 35, no. 3 (2016): 1541-1548. https://doi.org/10.3892/or.2016.4543
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