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Article

miR-410-3p suppresses breast cancer progression by targeting Snail

  • Authors:
    • Ya-Feng Zhang
    • Yue Yu
    • Wang-Zhao Song
    • Rui-Ming Zhang
    • Shan Jin
    • Jun-Wen Bai
    • Hong-Bin Kang
    • Xin Wang
    • Xu-Chen Cao
  • View Affiliations / Copyright

    Affiliations: The First Department of Breast Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Tianjin 300060, P.R. China, Key Laboratory of Cancer Prevention and Therapy, Tianjin 300060, P.R. China, Department of Surgery, Affiliated Hospital, Inner Mongolia Medical University, Inner Mongolia 010050, P.R. China
  • Pages: 480-486
    |
    Published online on: May 23, 2016
       https://doi.org/10.3892/or.2016.4828
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Abstract

miR-410-3p acts as an oncogene or tumor-suppressor gene in various types of cancer. However, its role in breast cancer remains unknown. In the present study, expression of miR-410-3p in 30 breast cancer and paired adjacent normal tissues was detected by RT-qPCR. The expression of miR-410-3p was downregulated in 76.7% of the breast cancer samples. To further validate the expression of miR-410-3p in breast cancer, we analyzed miR-410-3p expression profiling data set from The Cancer Genome Atlas (TCGA) including 683 breast cancer and 87 normal breast tissues. We observed that the expression of miR-410-3p was downregulated in breast cancer tissues. Next, we investigated the influence of miR-410-3p on cell proliferation by transiently transfecting the miR-410-3p mimic or inhibitor, as well as their corresponding controls in the MDA-MB-231 and MCF7 cell lines. miR-410-3p overexpression reduced cell growth, colony formation and the number of EdU-positive cells in the MDA-MB-231 cells. In contrast, inhibition of miR-410-3p in the MCF7 cells resulted in a higher proliferation rate as assessed by MTT assay, plate colony formation and EdU assays. Furthermore, miR-410-3p inhibited epithelial-mesenchymal transition. In addition, Snail was found to be a direct target of miR-410-3p based on a luciferase assay. Overexpression of Snail was able to rescue the effect of miR-410-3p in breast cancer cells. Moreover, miR‑410-3p was inversely expressed with Snail in breast cancer samples. Our data provide new knowledge regarding the role of miR-410-3p in breast cancer progression.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang Y, Yu Y, Song W, Zhang R, Jin S, Bai J, Kang H, Wang X and Cao X: miR-410-3p suppresses breast cancer progression by targeting Snail. Oncol Rep 36: 480-486, 2016.
APA
Zhang, Y., Yu, Y., Song, W., Zhang, R., Jin, S., Bai, J. ... Cao, X. (2016). miR-410-3p suppresses breast cancer progression by targeting Snail. Oncology Reports, 36, 480-486. https://doi.org/10.3892/or.2016.4828
MLA
Zhang, Y., Yu, Y., Song, W., Zhang, R., Jin, S., Bai, J., Kang, H., Wang, X., Cao, X."miR-410-3p suppresses breast cancer progression by targeting Snail". Oncology Reports 36.1 (2016): 480-486.
Chicago
Zhang, Y., Yu, Y., Song, W., Zhang, R., Jin, S., Bai, J., Kang, H., Wang, X., Cao, X."miR-410-3p suppresses breast cancer progression by targeting Snail". Oncology Reports 36, no. 1 (2016): 480-486. https://doi.org/10.3892/or.2016.4828
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang Y, Yu Y, Song W, Zhang R, Jin S, Bai J, Kang H, Wang X and Cao X: miR-410-3p suppresses breast cancer progression by targeting Snail. Oncol Rep 36: 480-486, 2016.
APA
Zhang, Y., Yu, Y., Song, W., Zhang, R., Jin, S., Bai, J. ... Cao, X. (2016). miR-410-3p suppresses breast cancer progression by targeting Snail. Oncology Reports, 36, 480-486. https://doi.org/10.3892/or.2016.4828
MLA
Zhang, Y., Yu, Y., Song, W., Zhang, R., Jin, S., Bai, J., Kang, H., Wang, X., Cao, X."miR-410-3p suppresses breast cancer progression by targeting Snail". Oncology Reports 36.1 (2016): 480-486.
Chicago
Zhang, Y., Yu, Y., Song, W., Zhang, R., Jin, S., Bai, J., Kang, H., Wang, X., Cao, X."miR-410-3p suppresses breast cancer progression by targeting Snail". Oncology Reports 36, no. 1 (2016): 480-486. https://doi.org/10.3892/or.2016.4828
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