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Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway

  • Authors:
    • Liang Peng
    • Yi Hu
    • Demeng Chen
    • Ruixia Linghu
    • Yingzhe Wang
    • Xiaoxue Kou
    • Junlan Yang
    • Shunchang Jiao
  • View Affiliations / Copyright

    Affiliations: Department of Oncology, Chinese PLA General Hospital, Beijing 100853, P.R. China, School of Dentistry, University of California, Los Angeles, CA 90095, USA
    Copyright: © Peng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4531-4537
    |
    Published online on: October 14, 2016
       https://doi.org/10.3892/ol.2016.5263
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Abstract

Ubiquitination and deubiquitination have emerged as critical regulators in cancer. In the present study, the expression pattern of 50 ubiquitin‑specific proteases (USPs) was summarized in breast cancer using a bioinformatics approach, and USP21 was identified as the most altered gene in breast cancer. In particular, expression of USP21 in triple negative breast cancer (TNBC) cell lines was greater compared with other subtypes of breast cancer. Knockdown of USP21 in TNBC cells inhibited cell proliferation, migration and invasion. Microarray profiling of the USP21 knockdown cells revealed significant downregulation of multiple genes associated with the NOD‑like receptor signaling pathway. The results of the present study suggest that USP21 has a significant role in TNBC progression, and therefore may represent a novel therapeutic target.
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Copy and paste a formatted citation
Spandidos Publications style
Peng L, Hu Y, Chen D, Linghu R, Wang Y, Kou X, Yang J and Jiao S: Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway. Oncol Lett 12: 4531-4537, 2016.
APA
Peng, L., Hu, Y., Chen, D., Linghu, R., Wang, Y., Kou, X. ... Jiao, S. (2016). Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway. Oncology Letters, 12, 4531-4537. https://doi.org/10.3892/ol.2016.5263
MLA
Peng, L., Hu, Y., Chen, D., Linghu, R., Wang, Y., Kou, X., Yang, J., Jiao, S."Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway". Oncology Letters 12.6 (2016): 4531-4537.
Chicago
Peng, L., Hu, Y., Chen, D., Linghu, R., Wang, Y., Kou, X., Yang, J., Jiao, S."Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway". Oncology Letters 12, no. 6 (2016): 4531-4537. https://doi.org/10.3892/ol.2016.5263
Copy and paste a formatted citation
x
Spandidos Publications style
Peng L, Hu Y, Chen D, Linghu R, Wang Y, Kou X, Yang J and Jiao S: Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway. Oncol Lett 12: 4531-4537, 2016.
APA
Peng, L., Hu, Y., Chen, D., Linghu, R., Wang, Y., Kou, X. ... Jiao, S. (2016). Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway. Oncology Letters, 12, 4531-4537. https://doi.org/10.3892/ol.2016.5263
MLA
Peng, L., Hu, Y., Chen, D., Linghu, R., Wang, Y., Kou, X., Yang, J., Jiao, S."Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway". Oncology Letters 12.6 (2016): 4531-4537.
Chicago
Peng, L., Hu, Y., Chen, D., Linghu, R., Wang, Y., Kou, X., Yang, J., Jiao, S."Ubiquitin specific protease 21 upregulation in breast cancer promotes cell tumorigenic capability and is associated with the NOD-like receptor signaling pathway". Oncology Letters 12, no. 6 (2016): 4531-4537. https://doi.org/10.3892/ol.2016.5263
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