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Article

Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells

  • Authors:
    • Ying Wang
    • Leqiu Wang
    • Changhao Yin
    • Baizhu An
    • Yankun Hao
    • Tao Wei
    • Li Li
    • Gaochen Song
  • View Affiliations / Copyright

    Affiliations: Medical Functional Laboratory, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China, Department of Otolaryngology, Hongqi Hospital of Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China, Department of Neurology, Hongqi Hospital of Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China, Department of Anatomy, Mudanjiang Medical University, Mudanjiang, Heilongjiang 157011, P.R. China
  • Pages: 1233-1238
    |
    Published online on: March 27, 2015
       https://doi.org/10.3892/mmr.2015.3558
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Abstract

Arsenic trioxide (As2O3) has been widely used in the treatment of acute promyelocytic leukemia and has been observed to exhibit therapeutic effects in various types of solid tumor. In a previous study by this group, it was shown that As2O3 induces the apoptosis of MCF‑7 breast cancer cells through inhibition of the human ether‑à‑go‑go‑related gene (hERG) channel. The present study was designed to further investigate the effect of As2O3 on breast cancer cells and to examine the mechanism underlying the regulation of hERG expression. The present study confirmed that As2O3 inhibited tumor growth in vivo, following MCF‑7 cell implantation into nude mice. Using computational prediction , it was identified that microRNA (miR)‑328 had a binding site in the 3'‑untranslated region of hERG mRNA. A luciferase activity assay demonstrated that hERG is a target gene of miR‑328. Further investigation using western blot analysis and reverse transcription‑quantitative polymerase chain reaction revealed that As2O3 downregulated hERG expression via upregulation of miR‑328 expression in MCF‑7 cells. In conclusion, As2O3 was observed to inhibit breast cancer cell growth, at least in part, through the miR‑328/hERG pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Wang Y, Wang L, Yin C, An B, Hao Y, Wei T, Li L and Song G: Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells. Mol Med Rep 12: 1233-1238, 2015.
APA
Wang, Y., Wang, L., Yin, C., An, B., Hao, Y., Wei, T. ... Song, G. (2015). Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells. Molecular Medicine Reports, 12, 1233-1238. https://doi.org/10.3892/mmr.2015.3558
MLA
Wang, Y., Wang, L., Yin, C., An, B., Hao, Y., Wei, T., Li, L., Song, G."Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells". Molecular Medicine Reports 12.1 (2015): 1233-1238.
Chicago
Wang, Y., Wang, L., Yin, C., An, B., Hao, Y., Wei, T., Li, L., Song, G."Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells". Molecular Medicine Reports 12, no. 1 (2015): 1233-1238. https://doi.org/10.3892/mmr.2015.3558
Copy and paste a formatted citation
x
Spandidos Publications style
Wang Y, Wang L, Yin C, An B, Hao Y, Wei T, Li L and Song G: Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells. Mol Med Rep 12: 1233-1238, 2015.
APA
Wang, Y., Wang, L., Yin, C., An, B., Hao, Y., Wei, T. ... Song, G. (2015). Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells. Molecular Medicine Reports, 12, 1233-1238. https://doi.org/10.3892/mmr.2015.3558
MLA
Wang, Y., Wang, L., Yin, C., An, B., Hao, Y., Wei, T., Li, L., Song, G."Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells". Molecular Medicine Reports 12.1 (2015): 1233-1238.
Chicago
Wang, Y., Wang, L., Yin, C., An, B., Hao, Y., Wei, T., Li, L., Song, G."Arsenic trioxide inhibits breast cancer cell growth via microRNA‑328/hERG pathway in MCF‑7 cells". Molecular Medicine Reports 12, no. 1 (2015): 1233-1238. https://doi.org/10.3892/mmr.2015.3558
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