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Article

miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6

  • Authors:
    • Qiming Hu
    • Jiacheng Song
    • Bo Ding
    • Yugui Cui
    • Jiale Liang
    • Suping Han
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210036, P.R. China, Department of Radiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210036, P.R. China, Department of Obstetrics and Gynecology, Zhongda Hospital, Medical School, Southeast University, Nanjing, Jiangsu 210009, P.R. China
  • Pages: 3015-3024
    |
    Published online on: April 23, 2018
       https://doi.org/10.3892/or.2018.6391
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Abstract

Cervical cancer is the third most common type of cancer in women, and microRNAs play an important role in this type of cancer. The elevated expression of miR-146a is involved in the pathogenesis of cancers generally, but its role in cervical cancer has not been fully elucidated. In the present study, we assessed the expression of miR-146a in G>C polymorphisms and confirmed that the overexpression of miR-146a promoted cervical cancer cell viability. The recombinant expression plasmids pre-miR-146a-G or pre-miR-146a-C including single nucleotide polymorphisms (SNP) were successfully constructed. Pre-miR-146a-G or pre-miR-146a-C was transfected into cervical cancer cells or immortalized non-tumorigenic cells and the expression of miR-146a was evaluated by real-time PCR. The cell viability, cell-cycle analysis and apoptosis were assessed using Cell Counting Kit-8 assay (CCK-8), flow cytometry and cleaved caspase-3 protein expression, respectively. The expression of interleukin 1 receptor associated kinase 1 (IRAK1), TNF receptor-associated factor 6 (TRAF6) and cyclin D1 was assessed following the transfection with a miR-146a mimic or a negative control. The cell viability and the number of S-phase cells increased after transfection with miR-146a mimic or an IRAK1 or TRAF6 interference fragment. After transfection, IRAK1 and TRAF6 protein expression was downregulated and the expression of cyclin D1 was upregulated, however apoptosis and cleaved caspase-3 were not affected. Polymorphisms in miR-146a precursor may be linked to the expression of miR-146a and may be a potential target for cervical cancer therapy.
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Copy and paste a formatted citation
Spandidos Publications style
Hu Q, Song J, Ding B, Cui Y, Liang J and Han S: miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6. Oncol Rep 39: 3015-3024, 2018.
APA
Hu, Q., Song, J., Ding, B., Cui, Y., Liang, J., & Han, S. (2018). miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6. Oncology Reports, 39, 3015-3024. https://doi.org/10.3892/or.2018.6391
MLA
Hu, Q., Song, J., Ding, B., Cui, Y., Liang, J., Han, S."miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6". Oncology Reports 39.6 (2018): 3015-3024.
Chicago
Hu, Q., Song, J., Ding, B., Cui, Y., Liang, J., Han, S."miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6". Oncology Reports 39, no. 6 (2018): 3015-3024. https://doi.org/10.3892/or.2018.6391
Copy and paste a formatted citation
x
Spandidos Publications style
Hu Q, Song J, Ding B, Cui Y, Liang J and Han S: miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6. Oncol Rep 39: 3015-3024, 2018.
APA
Hu, Q., Song, J., Ding, B., Cui, Y., Liang, J., & Han, S. (2018). miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6. Oncology Reports, 39, 3015-3024. https://doi.org/10.3892/or.2018.6391
MLA
Hu, Q., Song, J., Ding, B., Cui, Y., Liang, J., Han, S."miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6". Oncology Reports 39.6 (2018): 3015-3024.
Chicago
Hu, Q., Song, J., Ding, B., Cui, Y., Liang, J., Han, S."miR-146a promotes cervical cancer cell viability via targeting IRAK1 and TRAF6". Oncology Reports 39, no. 6 (2018): 3015-3024. https://doi.org/10.3892/or.2018.6391
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