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Article Open Access

miR-543 functions as a tumor suppressor in glioma in vitro and in vivo

  • Authors:
    • Liang Xu
    • Ju Yu
    • Zhongyong Wang
    • Qing Zhu
    • Wenjie Wang
    • Qing Lan
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215004, P.R. China, Cyrus Tang Hematology Center, Soochow University, Suzhou, Jiangsu 215123, P.R. China
    Copyright: © Xu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 725-734
    |
    Published online on: June 12, 2017
       https://doi.org/10.3892/or.2017.5712
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Abstract

Gliomas are the most common primary central nervous system tumors and account for approximately 80% of malignant brain tumors. MicroRNAs (miRNAs) are a class of small non-coding, regulatory RNA molecules that mediate the expression levels of specific proteins. As a member of the miRNA family, miR-543 plays a tumor suppressive or an oncogenic role in different types of tumors. However, the expression and role of miR-543 in glioma remain unknown. In the present study, the expression level of miR-543 in glioma cell lines and tissues was investigated. A series of in vitro and in vivo experiments was then performed to elucidate the function of miR-543 in glioma. Moreover, proteomic profiling was applied in this study to determine the landscape of differentially expressed proteins associated with miR-543-mediated carcinogenesis in glioma. We found that the expression level of miR-543 was greatly downregulated in glioma cell lines and tissues. Furthermore, the expression level of miR-543 was negatively associated with high-grade glioma. Functional studies demonstrated that miR-543 in glioma cells induced apoptosis and inhibited growth, the cell cycle, migration and invasion. In addition, the in vivo study showed that miR-543 suppressed tumorigenicity of glioma cells. In the present study, a label-free quantitative proteomic approach was performed and 339 proteins were identified as dysregulated after miR-543 was overexpressed. Among these dysregulated proteins, 165 were upregulated and 174 were downregulated. Moreover, multiple pathways were significantly enriched and were probably involved in miR-543-mediated tumorigenesis, including RNA degradation and the inositol phosphate metabolism pathway. In conclusion, miR-543 may function as a tumor suppressor in glioma and may serve as a future therapeutic target in therapy for patients with glioma.
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Copy and paste a formatted citation
Spandidos Publications style
Xu L, Yu J, Wang Z, Zhu Q, Wang W and Lan Q: miR-543 functions as a tumor suppressor in glioma in vitro and in vivo. Oncol Rep 38: 725-734, 2017.
APA
Xu, L., Yu, J., Wang, Z., Zhu, Q., Wang, W., & Lan, Q. (2017). miR-543 functions as a tumor suppressor in glioma in vitro and in vivo. Oncology Reports, 38, 725-734. https://doi.org/10.3892/or.2017.5712
MLA
Xu, L., Yu, J., Wang, Z., Zhu, Q., Wang, W., Lan, Q."miR-543 functions as a tumor suppressor in glioma in vitro and in vivo". Oncology Reports 38.2 (2017): 725-734.
Chicago
Xu, L., Yu, J., Wang, Z., Zhu, Q., Wang, W., Lan, Q."miR-543 functions as a tumor suppressor in glioma in vitro and in vivo". Oncology Reports 38, no. 2 (2017): 725-734. https://doi.org/10.3892/or.2017.5712
Copy and paste a formatted citation
x
Spandidos Publications style
Xu L, Yu J, Wang Z, Zhu Q, Wang W and Lan Q: miR-543 functions as a tumor suppressor in glioma in vitro and in vivo. Oncol Rep 38: 725-734, 2017.
APA
Xu, L., Yu, J., Wang, Z., Zhu, Q., Wang, W., & Lan, Q. (2017). miR-543 functions as a tumor suppressor in glioma in vitro and in vivo. Oncology Reports, 38, 725-734. https://doi.org/10.3892/or.2017.5712
MLA
Xu, L., Yu, J., Wang, Z., Zhu, Q., Wang, W., Lan, Q."miR-543 functions as a tumor suppressor in glioma in vitro and in vivo". Oncology Reports 38.2 (2017): 725-734.
Chicago
Xu, L., Yu, J., Wang, Z., Zhu, Q., Wang, W., Lan, Q."miR-543 functions as a tumor suppressor in glioma in vitro and in vivo". Oncology Reports 38, no. 2 (2017): 725-734. https://doi.org/10.3892/or.2017.5712
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