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MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1

  • Authors:
    • Xiaoping Rui
    • Haibin Zhao
    • Xianqiu Xiao
    • Li Wang
    • Lin Mo
    • Yao Yao
  • View Affiliations / Copyright

    Affiliations: Department of Thyroid Breast Surgery, Wuxi Taihu Hospital, Wuxi, Jiangsu 214044, P.R. China, Department of Pathology, Wuxi Taihu Hospital, Wuxi, Jiangsu 214044, P.R. China
    Copyright: © Rui et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 4387-4392
    |
    Published online on: September 17, 2018
       https://doi.org/10.3892/etm.2018.6744
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Abstract

MicroRNAs (miRs) have been reported to serve critical roles in the progression of tumors. However, thus far, the role of miR‑34a in breast cancer is largely unknown. Therefore, the present study aimed to investigate the expression and role of miR‑34a in breast cancer, and to further explore the underlying molecular mechanism. Reverse transcription‑quantitative polymerase chain reaction was performed to detect the level of miR‑34a in human breast cancer tissues. In addition, the role of miR‑34a in MCF‑7 breast cancer cells was investigated by performing miR‑34a overexpression or downregulation through transfection with miR‑34a mimic or inhibitor, respectively. Next, the viability and invasion of the MCF‑7 cells were respectively analyzed by MTT assay and transwell assay, while apoptosis and cell cycle progression were examined by flow cytometry. Furthermore, associated protein levels were measured using western blotting. The results demonstrated that miR‑34a was downregulated in human breast cancer tissues in comparison with the adjacent normal tissues. In addition, Notch1 was demonstrated to be a direct target of miR‑34a. miR‑34a mimic transfection inhibited MCF‑7 cell viability, induced cell apoptosis and G1 phase arrest, and prevented cell invasion, while miR‑34a inhibitor transfection resulted in the opposite effects. In conclusion, the presented data indicated that miR‑34a suppressed breast cancer cell proliferation and invasion, and its effect may partly be exerted by targeting Notch1.
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Copy and paste a formatted citation
Spandidos Publications style
Rui X, Zhao H, Xiao X, Wang L, Mo L and Yao Y: MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1. Exp Ther Med 16: 4387-4392, 2018.
APA
Rui, X., Zhao, H., Xiao, X., Wang, L., Mo, L., & Yao, Y. (2018). MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1. Experimental and Therapeutic Medicine, 16, 4387-4392. https://doi.org/10.3892/etm.2018.6744
MLA
Rui, X., Zhao, H., Xiao, X., Wang, L., Mo, L., Yao, Y."MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1". Experimental and Therapeutic Medicine 16.6 (2018): 4387-4392.
Chicago
Rui, X., Zhao, H., Xiao, X., Wang, L., Mo, L., Yao, Y."MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1". Experimental and Therapeutic Medicine 16, no. 6 (2018): 4387-4392. https://doi.org/10.3892/etm.2018.6744
Copy and paste a formatted citation
x
Spandidos Publications style
Rui X, Zhao H, Xiao X, Wang L, Mo L and Yao Y: MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1. Exp Ther Med 16: 4387-4392, 2018.
APA
Rui, X., Zhao, H., Xiao, X., Wang, L., Mo, L., & Yao, Y. (2018). MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1. Experimental and Therapeutic Medicine, 16, 4387-4392. https://doi.org/10.3892/etm.2018.6744
MLA
Rui, X., Zhao, H., Xiao, X., Wang, L., Mo, L., Yao, Y."MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1". Experimental and Therapeutic Medicine 16.6 (2018): 4387-4392.
Chicago
Rui, X., Zhao, H., Xiao, X., Wang, L., Mo, L., Yao, Y."MicroRNA‑34a suppresses breast cancer cell proliferation and invasion by targeting Notch1". Experimental and Therapeutic Medicine 16, no. 6 (2018): 4387-4392. https://doi.org/10.3892/etm.2018.6744
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