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Article

Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma

  • Authors:
    • Dong Chen
    • Xin Yu
  • View Affiliations / Copyright

    Affiliations: Department of Neurosurgery, Tianjin Huanhu Hospital, Tianjin 300350, P.R. China, Department of Surgery, Operating Room, Tianjin First Central Hospital, Tianjin 300192, P.R. China
    Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 5536-5544
    |
    Published online on: October 30, 2018
       https://doi.org/10.3892/mmr.2018.9609
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Abstract

Glioma is among the most common primary brain tumors and one of the most aggressive and lethal forms of human cancer. Long noncoding RNAs (lncRNAs) have demonstrated great importance in the development and progression of cancer. The present study aimed to investigate the role of the novel tumor suppressive lncRNA on Chromosome 8p12 (TSLNC8), in cell proliferation, metastasis and apoptosis in human glioma. It was initially reported that the relative transcript levels of TSLNC8 were significantly decreased in human glioma tissues and cultured glioma cells, as evidenced by RT‑qPCR. Among clinical variables, the expression of TSLNC8 was negatively associated with tumor size, distant metastasis, and tumor, node and metastasis stage. MTT assay demonstrated that overexpression of TSLNC8 in glioma cell lines U25‑MG and SWO38 decreased, whereas knockdown of TSLNC8 in glioma cells SHG‑44 and BT325 increased the cell proliferative rate over 5 consecutive days. Additionally, cell metastasis was inhibited in U251 and SWO38 cells when cells were transfected with TSLNC8‑expressing plasmid as observed via Transwell and wound‑healing assays. Furthermore, cell apoptotic rate was upregulated in TSLNC8 plasmid‑treated U251 and SWO38 cells, and inhibited by siRNA against TSLNC8 in SHG‑44 and BT325 cells by cell apoptotic assay. The relative activities of caspase‑3 and caspase‑9 were increased by TSLNC8 overexpression and decreased by TSLNC depletion; however, the activity of caspase‑8 remained unchanged. The results of the present study demonstrated the inhibitory effects of TSLNC8 in human glioma, which may contribute to advancement in the diagnosis and treatment of patients with glioma in clinic.
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Copy and paste a formatted citation
Spandidos Publications style
Chen D and Yu X: Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma. Mol Med Rep 18: 5536-5544, 2018.
APA
Chen, D., & Yu, X. (2018). Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma. Molecular Medicine Reports, 18, 5536-5544. https://doi.org/10.3892/mmr.2018.9609
MLA
Chen, D., Yu, X."Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma". Molecular Medicine Reports 18.6 (2018): 5536-5544.
Chicago
Chen, D., Yu, X."Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma". Molecular Medicine Reports 18, no. 6 (2018): 5536-5544. https://doi.org/10.3892/mmr.2018.9609
Copy and paste a formatted citation
x
Spandidos Publications style
Chen D and Yu X: Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma. Mol Med Rep 18: 5536-5544, 2018.
APA
Chen, D., & Yu, X. (2018). Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma. Molecular Medicine Reports, 18, 5536-5544. https://doi.org/10.3892/mmr.2018.9609
MLA
Chen, D., Yu, X."Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma". Molecular Medicine Reports 18.6 (2018): 5536-5544.
Chicago
Chen, D., Yu, X."Long noncoding RNA TSLNC8 suppresses cell proliferation and metastasis and promotes cell apoptosis in human glioma". Molecular Medicine Reports 18, no. 6 (2018): 5536-5544. https://doi.org/10.3892/mmr.2018.9609
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