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Article

Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL

  • Authors:
    • Xiaodong Lai
    • Yanchun Guo
    • Zhitao Guo
    • Ruibao Liu
    • Xunguo Wang
    • Fang Wang
  • View Affiliations / Copyright

    Affiliations: Department of Urology Surgery, Dongying People's Hospital, Dongying, Shandong, P.R. China, Department of Oncology Surgery, Dongying People's Hospital, Dongying, Shandong, P.R. China, Emergency Department, Tianjin Xiqing Hospital, Tianjin, P.R. China
  • Pages: 3651-3656
    |
    Published online on: October 24, 2016
       https://doi.org/10.3892/or.2016.5196
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Abstract

miR‑574‑5p has been reported involved in the pathogenesis of numerous human malignancies such as colorectal and lung cancer. In this study, we aimed to explore the roles of REL and miR‑574 in the recurrence of prostate cancer (PCa) and to identify the underlying molecular mechanisms. Our literature search found that miR‑574 is regulated in cancer stem cells (CSCs), and next we used the microRNA (miRNA) database (www.mirdb.org) to find REL as a target of miR‑574. Luciferase assay was performed to verify the miRNA/target relationship. Oligo-transfection, real‑time PCR and western blot analysis were used to support the conclusions. We validated REL to be the direct gene via luciferase reporter assay system, and real‑time PCR and western blot analysis were also conducted to study the mRNA and protein expression level of REL between different groups (recurrence and non‑recurrence) or cells treated with scramble control, miR‑574 mimics, REL siRNA and miR‑574 inhibitors, indicating the negative regulatory relationship between miR‑574 and REL. We also investigated the relative viability of prostate CSCs when transfected with scramble control, miR‑574 mimics, REL siRNA and miR‑574 inhibitors to validate miR‑574 to be positively interfering with the viability of prostate CSCs. We then investigated the relative apoptosis of prostate CSCs when transfected with scramble control, miR‑574 mimics, REL siRNA and miR‑574 inhibitors. The results showed miR‑574 inhibited apoptosis. In conclusion, miR‑574 might be a novel prognostic and therapeutic target in the management of PCa recurrence.
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Copy and paste a formatted citation
Spandidos Publications style
Lai X, Guo Y, Guo Z, Liu R, Wang X and Wang F: Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL. Oncol Rep 36: 3651-3656, 2016.
APA
Lai, X., Guo, Y., Guo, Z., Liu, R., Wang, X., & Wang, F. (2016). Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL. Oncology Reports, 36, 3651-3656. https://doi.org/10.3892/or.2016.5196
MLA
Lai, X., Guo, Y., Guo, Z., Liu, R., Wang, X., Wang, F."Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL". Oncology Reports 36.6 (2016): 3651-3656.
Chicago
Lai, X., Guo, Y., Guo, Z., Liu, R., Wang, X., Wang, F."Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL". Oncology Reports 36, no. 6 (2016): 3651-3656. https://doi.org/10.3892/or.2016.5196
Copy and paste a formatted citation
x
Spandidos Publications style
Lai X, Guo Y, Guo Z, Liu R, Wang X and Wang F: Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL. Oncol Rep 36: 3651-3656, 2016.
APA
Lai, X., Guo, Y., Guo, Z., Liu, R., Wang, X., & Wang, F. (2016). Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL. Oncology Reports, 36, 3651-3656. https://doi.org/10.3892/or.2016.5196
MLA
Lai, X., Guo, Y., Guo, Z., Liu, R., Wang, X., Wang, F."Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL". Oncology Reports 36.6 (2016): 3651-3656.
Chicago
Lai, X., Guo, Y., Guo, Z., Liu, R., Wang, X., Wang, F."Downregulation of microRNA‑574 in cancer stem cells causes recurrence of prostate cancer via targeting REL". Oncology Reports 36, no. 6 (2016): 3651-3656. https://doi.org/10.3892/or.2016.5196
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