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Article Open Access

miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3

  • Authors:
    • Wu Xiang
    • Haotian Lin
    • Qilin Wang
    • Wan Chen
    • Zhaochuan Liu
    • Hui Chen
    • Hui Zhang
    • Weirong Chen
  • View Affiliations / Copyright

    Affiliations: State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat‑Sen University, Guangzhou, Guangdong 510060, P.R. China, Institute of Human Virology, Zhongshan School of Medicine, Sun Yat‑Sen University, Guangzhou, Guangdong 510074, P.R. China
    Copyright: © Xiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5049-5056
    |
    Published online on: October 27, 2016
       https://doi.org/10.3892/mmr.2016.5901
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Abstract

microRNA (miRNA) is abnormally expressed in numerous diseases, and it was intimately associated with cell proliferation and apoptosis. However, the mechanism by which miRNAs control cataractogenesis remains unclear. In the current study, it was demonstrated that miR‑34a was highly expressed in the cataractous lens by stem‑loop reverse transcription‑quantitative polymerase chain reaction. Trying to investigate the role of miR‑34a in human lens epithelial cells, miR‑34a mimics were transfected into SRA01/04 cells, and this suppressed proliferation and induced apoptosis. Subsequently, E2F3 was confirmed as a direct target of miR‑34a. Downregulation of E2F3 by small interfering (si) RNA siE2F3 resulted in proliferation inhibition and apoptosis of SRA01/04 cells. Furthermore, it was demonstrated that miR‑34a and siE2F3 downregulated E2F3 expression at a protein level. In summary, the current study demonstrated that miR‑34a suppressed the proliferation and induced apoptosis of SRA01/04 cells by downregulating E2F3. These observations provide novel insights with potential therapeutic applications for the treatment of cataracts.
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Copy and paste a formatted citation
Spandidos Publications style
Xiang W, Lin H, Wang Q, Chen W, Liu Z, Chen H, Zhang H and Chen W: miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3. Mol Med Rep 14: 5049-5056, 2016.
APA
Xiang, W., Lin, H., Wang, Q., Chen, W., Liu, Z., Chen, H. ... Chen, W. (2016). miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3. Molecular Medicine Reports, 14, 5049-5056. https://doi.org/10.3892/mmr.2016.5901
MLA
Xiang, W., Lin, H., Wang, Q., Chen, W., Liu, Z., Chen, H., Zhang, H., Chen, W."miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3". Molecular Medicine Reports 14.6 (2016): 5049-5056.
Chicago
Xiang, W., Lin, H., Wang, Q., Chen, W., Liu, Z., Chen, H., Zhang, H., Chen, W."miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3". Molecular Medicine Reports 14, no. 6 (2016): 5049-5056. https://doi.org/10.3892/mmr.2016.5901
Copy and paste a formatted citation
x
Spandidos Publications style
Xiang W, Lin H, Wang Q, Chen W, Liu Z, Chen H, Zhang H and Chen W: miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3. Mol Med Rep 14: 5049-5056, 2016.
APA
Xiang, W., Lin, H., Wang, Q., Chen, W., Liu, Z., Chen, H. ... Chen, W. (2016). miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3. Molecular Medicine Reports, 14, 5049-5056. https://doi.org/10.3892/mmr.2016.5901
MLA
Xiang, W., Lin, H., Wang, Q., Chen, W., Liu, Z., Chen, H., Zhang, H., Chen, W."miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3". Molecular Medicine Reports 14.6 (2016): 5049-5056.
Chicago
Xiang, W., Lin, H., Wang, Q., Chen, W., Liu, Z., Chen, H., Zhang, H., Chen, W."miR‑34a suppresses proliferation and induces apoptosis of human lens epithelial cells by targeting E2F3". Molecular Medicine Reports 14, no. 6 (2016): 5049-5056. https://doi.org/10.3892/mmr.2016.5901
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