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MicroRNA‑1291 mediates cell proliferation and tumorigenesis by downregulating MED1 in prostate cancer

  • Authors:
    • Qi Cai
    • An Zhao
    • Ligang Ren
    • Jing Chen
    • Kaisen Liao
    • Zhanshi Wang
    • Wei Zhang

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  • Published online on: January 28, 2019     https://doi.org/10.3892/ol.2019.9980
  • Pages: 3253-3260

  • Copyright: © Cai et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

miRNAs are important factors involved in the regulation of tumor development. miR‑1291 was found to have regulatory effects in many tumors, but its role in prostate cancer (PCa) still remains unclear. We explored the expression of miR‑1291 in PCa to reveal its role in regulating the progression of PCa as well as its underlying mechanism. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to detect the expression of miR‑1291 in PCa tissues and cell lines compared to normal tissues and cell lines. miR‑1291 mimics and inhibitors were applied to overexpress or inhibit the level of miR‑1291 in PCa cells. The ability of cell proliferation was measured using MTT assay, and cell cycle distribution was determined by flow cytometry. The potential target of miR‑1291 was identified via western blot analysis and luciferase assays. Then a xenograft model was established to explore the function of miR‑1291 in PCa in vivo. The results revealed that the expression level of miR‑1291 was significantly lower in the PCa tissues than that in the normal adjacent tissues. In PCa‑derived cells, there was also a downregulated expression level of miR‑1291. Overexpression of miR‑1291 obviously inhibited DU‑145 cell proliferation and induced cell cycle transition from G0/G1 to S phase. However, inhibition of miR‑1291 promoted the growth of LNCaP cells, and promoted the cell cycle transition to S phase and G2/M phase. MED1 was proven to be a potential target gene of miR‑1291, and miR‑1291 significantly inhibited its expression. At the in vivo level, overexpression of miR‑1291 inhibited the growth of xenograft tumors and significantly inhibited the expression of MED1 protein. Our study demonstrated that miR‑1291 inhibits cell proliferation and tumorigenesis of PCa via MED1, which might provide a novel target for PCa diagnosis and biological therapy.
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March-2019
Volume 17 Issue 3

Print ISSN: 1792-1074
Online ISSN:1792-1082

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  • CiteScore: 6.3
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  • Source Normalized Impact per Paper (SNIP): 0.725
  • SCImago Journal Rank (SJR): 0.639
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Spandidos Publications style
Cai Q, Zhao A, Ren L, Chen J, Liao K, Wang Z and Zhang W: MicroRNA‑1291 mediates cell proliferation and tumorigenesis by downregulating MED1 in prostate cancer . Oncol Lett 17: 3253-3260, 2019
APA
Cai, Q., Zhao, A., Ren, L., Chen, J., Liao, K., Wang, Z., & Zhang, W. (2019). MicroRNA‑1291 mediates cell proliferation and tumorigenesis by downregulating MED1 in prostate cancer . Oncology Letters, 17, 3253-3260. https://doi.org/10.3892/ol.2019.9980
MLA
Cai, Q., Zhao, A., Ren, L., Chen, J., Liao, K., Wang, Z., Zhang, W."MicroRNA‑1291 mediates cell proliferation and tumorigenesis by downregulating MED1 in prostate cancer ". Oncology Letters 17.3 (2019): 3253-3260.
Chicago
Cai, Q., Zhao, A., Ren, L., Chen, J., Liao, K., Wang, Z., Zhang, W."MicroRNA‑1291 mediates cell proliferation and tumorigenesis by downregulating MED1 in prostate cancer ". Oncology Letters 17, no. 3 (2019): 3253-3260. https://doi.org/10.3892/ol.2019.9980