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Article

Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle

  • Authors:
    • Mei Yang
    • Hongwen Gao
    • Peng Chen
    • Jiaoyuan Jia
    • Shan Wu
  • View Affiliations / Copyright

    Affiliations: Department of Pathology, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China
  • Pages: 171-178
    |
    Published online on: April 26, 2013
       https://doi.org/10.3892/or.2013.2428
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Abstract

Interferon-induced transmembrane protein 3 (IFITM3) is an important anti-virus protein and has been recently shown to play a role in human cancer development. Thus, the present study aimed to assess the expression of the IFITM3 protein in breast cancer tissues and to investigate the in vitro effects of IFITM3 knockdown in the regulation of breast cancer cell growth and cell cycle distributions. A total of 64 patients of breast cancer and the matched normal tissue specimens were obtained for immunohistochemical analysis of IFITM3 expression. Lentivirus-carrying IFITM3 shRNA was used to knock down IFITM3 expression in breast cancer cell lines. Phenotypic changes of cell viability, growth, colony formation and cell cycle distribution was also assayed using flow cytometry, MTT, BrdU incorporation and colony formation assays. The IFITM3 protein was highly expressed in invasive breast cancer compared to normal tissues and was significantly associated with estrogen receptor and progesterone receptor status. The lentivirus-carried IFITM3 shRNA significantly reduced the expression of IFITM3 mRNA and protein in breast cancer cells, inhibiting tumor cell viability, growth and colony formation, arrested tumor cells at the G0/G1 phase of the cell cycle and reduced the number of cells in the S phase of the cell cycle. Expression of IFITM3 protein could be a potential therapeutic target in future treatment of breast cancer.
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Copy and paste a formatted citation
Spandidos Publications style
Yang M, Gao H, Chen P, Jia J and Wu S: Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle. Oncol Rep 30: 171-178, 2013.
APA
Yang, M., Gao, H., Chen, P., Jia, J., & Wu, S. (2013). Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle. Oncology Reports, 30, 171-178. https://doi.org/10.3892/or.2013.2428
MLA
Yang, M., Gao, H., Chen, P., Jia, J., Wu, S."Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle". Oncology Reports 30.1 (2013): 171-178.
Chicago
Yang, M., Gao, H., Chen, P., Jia, J., Wu, S."Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle". Oncology Reports 30, no. 1 (2013): 171-178. https://doi.org/10.3892/or.2013.2428
Copy and paste a formatted citation
x
Spandidos Publications style
Yang M, Gao H, Chen P, Jia J and Wu S: Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle. Oncol Rep 30: 171-178, 2013.
APA
Yang, M., Gao, H., Chen, P., Jia, J., & Wu, S. (2013). Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle. Oncology Reports, 30, 171-178. https://doi.org/10.3892/or.2013.2428
MLA
Yang, M., Gao, H., Chen, P., Jia, J., Wu, S."Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle". Oncology Reports 30.1 (2013): 171-178.
Chicago
Yang, M., Gao, H., Chen, P., Jia, J., Wu, S."Knockdown of interferon-induced transmembrane protein 3 expression suppresses breast cancer cell growth and colony formation and affects the cell cycle". Oncology Reports 30, no. 1 (2013): 171-178. https://doi.org/10.3892/or.2013.2428
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