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Article Open Access

miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2

  • Authors:
    • Bifan Deng
    • Feiqun Su
    • Ruibin Xie
    • Weiguang Tang
  • View Affiliations / Copyright

    Affiliations: Department of Otorhinolaryngology, Head and Neck Surgery, Hezhou Renmin Hospital, Hezhou, Guangxi 542899, P.R. China, Department of Nursing, Hezhou Renmin Hospital, Hezhou, Guangxi 542899, P.R. China, Department of Cardiovascular Medicine, Hezhou Renmin Hospital, Hezhou, Guangxi 542899, P.R. China, Department of Nephrology and Rheumatology, Hezhou Renmin Hospital, Hezhou, Guangxi 542899, P.R. China
    Copyright: © Deng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 9209-9215
    |
    Published online on: April 12, 2018
       https://doi.org/10.3892/ol.2018.8481
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Abstract

The aim of the present study was to investigate the expression and function of microRNA (miR)‑371‑5p in nasopharyngeal carcinoma (NPC). The levels of miR‑371‑5p were analyzed in nasopharyngeal epithelium tissues, NPC tissues, human NPC cell lines and NP69 cells using reverse transcription‑quantitative polymerase chain reaction analysis. The association between the level of miR‑371‑5p and clinicopathological variables was also investigated. Cell proliferation was determined using an MTT assay, and the activities of cell metastasis were determined using wound healing and Transwell migration assays. To assess whether miR‑371‑5p can combine with the targeting sequence of B‑cell lymphoma 2 (BCL2) mRNA or not, a luciferase activity assay was performed. An animal experiment was used to examine the effect of miR‑371‑5p on the development of NPC. The results revealed that the expression of miR‑371‑5p was reduced in NPC samples and NPC cells. The level of miR‑371‑5p was associated with clinical stage and distant metastasis in patients with NPC, and was inversely associated with the protein level of BCL‑2 in NPC tissues. The upregulation of miR‑371‑5p reduced cell growth, migration and invasion, and inhibited carcinoma growth through targeting BCL2 mRNA. Taken together, the regulation of miR‑371‑5p was shown to offer potential as a novel treatment approach for NPC.
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Copy and paste a formatted citation
Spandidos Publications style
Deng B, Su F, Xie R and Tang W: miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2. Oncol Lett 15: 9209-9215, 2018.
APA
Deng, B., Su, F., Xie, R., & Tang, W. (2018). miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2. Oncology Letters, 15, 9209-9215. https://doi.org/10.3892/ol.2018.8481
MLA
Deng, B., Su, F., Xie, R., Tang, W."miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2". Oncology Letters 15.6 (2018): 9209-9215.
Chicago
Deng, B., Su, F., Xie, R., Tang, W."miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2". Oncology Letters 15, no. 6 (2018): 9209-9215. https://doi.org/10.3892/ol.2018.8481
Copy and paste a formatted citation
x
Spandidos Publications style
Deng B, Su F, Xie R and Tang W: miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2. Oncol Lett 15: 9209-9215, 2018.
APA
Deng, B., Su, F., Xie, R., & Tang, W. (2018). miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2. Oncology Letters, 15, 9209-9215. https://doi.org/10.3892/ol.2018.8481
MLA
Deng, B., Su, F., Xie, R., Tang, W."miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2". Oncology Letters 15.6 (2018): 9209-9215.
Chicago
Deng, B., Su, F., Xie, R., Tang, W."miR‑371‑5p suppresses the proliferative and migratory capacity of human nasopharyngeal carcinoma by targeting BCL2". Oncology Letters 15, no. 6 (2018): 9209-9215. https://doi.org/10.3892/ol.2018.8481
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