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Article Open Access

Tumor promoter role of miR‑647 in gastric cancer via repression of TP73

  • Authors:
    • Xiangqian Zhang
    • Min Zhang
    • Guifeng Wang
    • Ye Tian
    • Xiaolong He
  • View Affiliations / Copyright

    Affiliations: College of Life Sciences, Yan'an University, Yanan, Shaanxi 716000, P.R. China
    Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 3744-3750
    |
    Published online on: August 6, 2018
       https://doi.org/10.3892/mmr.2018.9358
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Abstract

It has previously been demonstrated that miRNA (miR)‑647 exhibits an important role in various cancers, and is aberrantly expressed in gastric cancer (GC). However, the exact role of miR‑647 in GC still remains unclear. The present study aimed to investigate the functional significance of miR‑647 and its target gene in GC. TargetScan and Miranda databases were used to predict the putative targets, and the prediction was validated by Dual‑luciferase Reporter Assays. To investigate whether miR‑647 affects GC cell behavior, a stable miR‑647‑overexpression/low‑expression cell line was generated by transfection with miR‑647 mimic/inhibitor. MTT, Flow Cytometry and Transwell invasion assays were performed to investigate the proliferation, cell apoptosis, migration and invasion properties of MGC‑803 cells. Additionally, reverse transcription‑quantitative polymerase chain reaction and western blot analysis were performed to detect the mRNA and protein expression levels of the apoptosis‑associated genes. The results suggested that tumor protein P73 (TP73) is a target gene of miR‑647. TP73 was markedly decreased following miR‑647 overexpression and significantly increased following miR‑647 inhibition. Following overexpression of miR‑647, the proliferation, migration and invasion of MGC‑803 cells were significantly increased, whereas the percentage of apoptotic cells decreased. Conversely, the proliferation, migration and invasion of MGC‑803 cells were significantly declined, and the percentage of apoptotic cells increased following miR‑647 inhibition. In addition, the B cell lymphoma (Bcl)‑2 Associated X, Apoptosis Regulator/Bcl‑2 ratio was markedly decreased when miR‑647 was overexpressed by miRNA mimics, and significantly increased when miR‑647 expression was inhibited via an miRNA inhibitor. Overall, miR‑647 functions as a tumor promoter in GC by repressing TP73.
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Copy and paste a formatted citation
Spandidos Publications style
Zhang X, Zhang M, Wang G, Tian Y and He X: Tumor promoter role of miR‑647 in gastric cancer via repression of TP73. Mol Med Rep 18: 3744-3750, 2018.
APA
Zhang, X., Zhang, M., Wang, G., Tian, Y., & He, X. (2018). Tumor promoter role of miR‑647 in gastric cancer via repression of TP73. Molecular Medicine Reports, 18, 3744-3750. https://doi.org/10.3892/mmr.2018.9358
MLA
Zhang, X., Zhang, M., Wang, G., Tian, Y., He, X."Tumor promoter role of miR‑647 in gastric cancer via repression of TP73". Molecular Medicine Reports 18.4 (2018): 3744-3750.
Chicago
Zhang, X., Zhang, M., Wang, G., Tian, Y., He, X."Tumor promoter role of miR‑647 in gastric cancer via repression of TP73". Molecular Medicine Reports 18, no. 4 (2018): 3744-3750. https://doi.org/10.3892/mmr.2018.9358
Copy and paste a formatted citation
x
Spandidos Publications style
Zhang X, Zhang M, Wang G, Tian Y and He X: Tumor promoter role of miR‑647 in gastric cancer via repression of TP73. Mol Med Rep 18: 3744-3750, 2018.
APA
Zhang, X., Zhang, M., Wang, G., Tian, Y., & He, X. (2018). Tumor promoter role of miR‑647 in gastric cancer via repression of TP73. Molecular Medicine Reports, 18, 3744-3750. https://doi.org/10.3892/mmr.2018.9358
MLA
Zhang, X., Zhang, M., Wang, G., Tian, Y., He, X."Tumor promoter role of miR‑647 in gastric cancer via repression of TP73". Molecular Medicine Reports 18.4 (2018): 3744-3750.
Chicago
Zhang, X., Zhang, M., Wang, G., Tian, Y., He, X."Tumor promoter role of miR‑647 in gastric cancer via repression of TP73". Molecular Medicine Reports 18, no. 4 (2018): 3744-3750. https://doi.org/10.3892/mmr.2018.9358
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