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Article

MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor

  • Authors:
    • Xin Rui
    • Ting‑Ting Gu
    • Hua‑Feng Pan
    • Si‑Liang Shao
    • Hong‑Xiang Shao
  • View Affiliations / Copyright

    Affiliations: Department of Urology, HwaMei Hospital, University of Chinese Academy of Sciences (Ningbo No. 2 Hospital), Ningbo, Zhejiang 315010, P.R. China
  • Pages: 2066-2072
    |
    Published online on: June 12, 2019
       https://doi.org/10.3892/ol.2019.10471
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Abstract

Prostate cancer (PCa) is the most frequently diagnosed malignancy in men and its incidence has increased rapidly worldwide. Notably, the molecular mechanisms underlying prostate tumorigenesis have not been fully identified. The levels of microRNA (miR)‑381 have been explored in numerous types of malignancy; however, the expression levels and biological function of miR‑381 in PCa remain largely unknown. In the present study, reverse‑transcription polymerase chain reaction was used to detect the expression levels of miR‑381 in PCa cells and normal prostate epithelial cells. Subsequently, miR‑381 antisense oligonucleotides and mimics were transfected into LNCaP PCa cells. Bioinformatics analysis was performed to identify the potential target genes of miR‑381. Protein expression analysis, dual‑luciferase reporter assay and a rescue assay were used to confirm the target of miR‑381. The data suggested that the expression levels of miR‑381 were significantly decreased in PCa cells compared with in normal prostatic epithelial cells. Furthermore, transfection of LNCaP cells with miR‑381 mimics suppressed their proliferation, migration and invasion. In addition, bioinformatics analysis suggested that the androgen receptor (AR) was a target gene of miR‑381. miR‑381 suppressed the expression levels of AR by directly binding to its 3'‑untranslated region. Furthermore, transfection with an AR plasmid partially attenuated miR‑381‑induced inhibition of cell proliferation, migration and invasion. The results of the present study suggested that miR‑381 may act as a tumor suppressor in PCa by directly targeting the AR.
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Copy and paste a formatted citation
Spandidos Publications style
Rui X, Gu TT, Pan HF, Shao SL and Shao HX: MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor. Oncol Lett 18: 2066-2072, 2019.
APA
Rui, X., Gu, T., Pan, H., Shao, S., & Shao, H. (2019). MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor. Oncology Letters, 18, 2066-2072. https://doi.org/10.3892/ol.2019.10471
MLA
Rui, X., Gu, T., Pan, H., Shao, S., Shao, H."MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor". Oncology Letters 18.2 (2019): 2066-2072.
Chicago
Rui, X., Gu, T., Pan, H., Shao, S., Shao, H."MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor". Oncology Letters 18, no. 2 (2019): 2066-2072. https://doi.org/10.3892/ol.2019.10471
Copy and paste a formatted citation
x
Spandidos Publications style
Rui X, Gu TT, Pan HF, Shao SL and Shao HX: MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor. Oncol Lett 18: 2066-2072, 2019.
APA
Rui, X., Gu, T., Pan, H., Shao, S., & Shao, H. (2019). MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor. Oncology Letters, 18, 2066-2072. https://doi.org/10.3892/ol.2019.10471
MLA
Rui, X., Gu, T., Pan, H., Shao, S., Shao, H."MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor". Oncology Letters 18.2 (2019): 2066-2072.
Chicago
Rui, X., Gu, T., Pan, H., Shao, S., Shao, H."MicroRNA‑381 suppresses proliferation and invasion of prostate cancer cells through downregulation of the androgen receptor". Oncology Letters 18, no. 2 (2019): 2066-2072. https://doi.org/10.3892/ol.2019.10471
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