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miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma

  • Authors:
    • Jun Xin
    • Li‑Min Zheng
    • De‑Ke Sun
    • Xian‑Feng Li
    • Peng Xu
    • Li‑Qiang Tian
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, Yishui Central Hospital, Linyi, Shandong 276400, P.R. China, Department of Neurosurgery, Tai'an Central Hospital, Tai'an, Shandong 271000, P.R. China, Department of Neurosurgery, Linyi People's Hospital, Linyi, Shandong 276003, P.R. China
    Copyright: © Xin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1439-1448
    |
    Published online on: May 30, 2018
       https://doi.org/10.3892/ol.2018.8846
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Abstract

Gliomas are the most common type of malignant primary brain tumors in adults and exhibit a spectrum of aberrantly aggressive phenotypes. Despite advances in treatments during past decades, prognosis of the disease remains poor, with a median survival time of 12‑14 months. Future studies on the molecular mechanism of the disease may provide the theoretical basis to identify new targets for effective therapies. The present study revealed that in glioblastoma cells, the overexpression of cytochrome P450, family 27, subfamily A, polypeptide 1 (CYP27A1) promoted proliferation, while silencing of CYP27A1 inhibited proliferation, without affecting migration and invasion. CYP27A1 protein was upregulated in glioblastoma tissues, indicating that CYP27A1 is an oncogene. The downregulation of specific microRNAs (miRNA) may contribute to the upregulation of oncogenes in glioblastoma. A common strategy was used to predict target miRNAs of CPY27A1 using the miRanda algorithm. miR‑211 and miR‑204 could target the 3'untranslated region of CPY27A1 mRNA. Additional studies confirmed that the overexpression of miR‑204 inhibited CPY27A1 expression in glioblastoma cells. Finally, it was identified that miR‑204 was downregulated in glioblastoma and that its overexpression inhibited proliferation, migration and invasion in glioblastoma cells. Thus, it was concluded that miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma.
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Copy and paste a formatted citation
Spandidos Publications style
Xin J, Zheng LM, Sun DK, Li XF, Xu P and Tian LQ: miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma. Oncol Lett 16: 1439-1448, 2018.
APA
Xin, J., Zheng, L., Sun, D., Li, X., Xu, P., & Tian, L. (2018). miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma. Oncology Letters, 16, 1439-1448. https://doi.org/10.3892/ol.2018.8846
MLA
Xin, J., Zheng, L., Sun, D., Li, X., Xu, P., Tian, L."miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma". Oncology Letters 16.2 (2018): 1439-1448.
Chicago
Xin, J., Zheng, L., Sun, D., Li, X., Xu, P., Tian, L."miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma". Oncology Letters 16, no. 2 (2018): 1439-1448. https://doi.org/10.3892/ol.2018.8846
Copy and paste a formatted citation
x
Spandidos Publications style
Xin J, Zheng LM, Sun DK, Li XF, Xu P and Tian LQ: miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma. Oncol Lett 16: 1439-1448, 2018.
APA
Xin, J., Zheng, L., Sun, D., Li, X., Xu, P., & Tian, L. (2018). miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma. Oncology Letters, 16, 1439-1448. https://doi.org/10.3892/ol.2018.8846
MLA
Xin, J., Zheng, L., Sun, D., Li, X., Xu, P., Tian, L."miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma". Oncology Letters 16.2 (2018): 1439-1448.
Chicago
Xin, J., Zheng, L., Sun, D., Li, X., Xu, P., Tian, L."miR‑204 functions as a tumor suppressor gene, at least partly by suppressing CYP27A1 in glioblastoma". Oncology Letters 16, no. 2 (2018): 1439-1448. https://doi.org/10.3892/ol.2018.8846
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