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Article

MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2

  • Authors:
    • Rui Li
    • Hongxia Zhang
    • Xiling Zheng
  • View Affiliations / Copyright

    Affiliations: Department of Otorhinolaryngology, Hospital of Laiwu Iron and Steel Group Company, Laiwu, Shandong 271100, P.R. China, Department of ENT, Hanzhong 3201 Hospital Affiliated to Xi'an Jiaotong University of Medicine, Hanzhong, Shaanxi 723000, P.R. China, Department of Otorhinolaryngology, Yanan University Affiliated Hospital, Yanan, Shaanxi 716000, P.R. China
  • Pages: 3357-3361
    |
    Published online on: December 19, 2017
       https://doi.org/10.3892/ol.2017.7640
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Abstract

The present study aimed to investigate microRNA (miR/miRNA)-34c expression and the association of miR‑34c with B cell lymphoma 2 (BCL2) in M4e laryngeal carcinoma cell line. M4e laryngeal carcinoma cells were cultured and transfected with lenti‑miR‑34c or scramble miRNA for 72 h. Cell viability and the percentage of cells undergoing apoptosis of transfected cells were detected using MTT and Annexin V/allophycocyanin and propidium iodide assays, respectively. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis were performed to determine BCL2 mRNA and protein expression in transfected M4e cells. In addition, luciferase reporter assay was performed to identify whether BCL2 is a direct target of miR‑34c. Transfection of lenti‑miR‑34c was able to significantly inhibit cell viability (P<0.01), increase the percentage of cells undergoing apoptosis (P<0.001) and downregulate BCL2 protein expression (P<0.01) in M4e cells. RT‑qPCR data revealed that lenti‑miR‑34c transfection did not affect BCL2 mRNA expression. However, data from the luciferase reporter assay revealed that transfection with miR‑34c negative control decreased luciferase activity in M4e cells co‑transfected with pGL3‑BCL2‑MUT plasmid, compared with miR‑34c inhibitor (P<0.01). Collectively, the results from the present study provided evidence that miR‑34c may be involved in the pathogenesis of laryngeal cancer, and BCL2 may be negatively regulated by miR‑34c in M4e cells.
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Copy and paste a formatted citation
Spandidos Publications style
Li R, Zhang H and Zheng X: MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2. Oncol Lett 15: 3357-3361, 2018.
APA
Li, R., Zhang, H., & Zheng, X. (2018). MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2. Oncology Letters, 15, 3357-3361. https://doi.org/10.3892/ol.2017.7640
MLA
Li, R., Zhang, H., Zheng, X."MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2". Oncology Letters 15.3 (2018): 3357-3361.
Chicago
Li, R., Zhang, H., Zheng, X."MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2". Oncology Letters 15, no. 3 (2018): 3357-3361. https://doi.org/10.3892/ol.2017.7640
Copy and paste a formatted citation
x
Spandidos Publications style
Li R, Zhang H and Zheng X: MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2. Oncol Lett 15: 3357-3361, 2018.
APA
Li, R., Zhang, H., & Zheng, X. (2018). MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2. Oncology Letters, 15, 3357-3361. https://doi.org/10.3892/ol.2017.7640
MLA
Li, R., Zhang, H., Zheng, X."MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2". Oncology Letters 15.3 (2018): 3357-3361.
Chicago
Li, R., Zhang, H., Zheng, X."MiR-34c induces apoptosis and inhibits the viability of M4e cells by targeting BCL2". Oncology Letters 15, no. 3 (2018): 3357-3361. https://doi.org/10.3892/ol.2017.7640
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