Open Access

miR‑138‑5p suppresses glioblastoma cell viability and leads to cell cycle arrest by targeting cyclin D3

  • Authors:
    • Henggang Wu
    • Cheng Wang
    • Yajun Liu
    • Chao Yang
    • Xiaolong Liang
    • Xin Zhang
    • Xu Li
  • View Affiliations

  • Published online on: September 21, 2020     https://doi.org/10.3892/ol.2020.12127
  • Article Number: 264
  • Copyright: © Wu et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

Metrics: Total Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )


Abstract

Although malignant glioblastoma (GBM) treatment has significantly improved in the past few decades, the prognosis of GBM remains unsatisfactory. MicroRNA (miR)‑138‑5p has been reported as a tumor suppressor in several types of human cancer; however, little is known about the function of miR‑138‑5p in GBM. The present study aimed to investigate the role of miR‑138‑5p in GBM as well as the underlying molecular mechanisms. The present study performed bioinformatics analysis, reverse transcription‑quantitative (RT‑q)PCR, western blotting, cell viability assays, colony formation assays, invasion assays and cell cycle analysis to investigate the biological function of miR‑138‑5p in both patient tissues and cell lines. In addition, miR‑138‑5p targets in GBM were predicted using Gene Expression Omnibus website and further validated by a dual luciferase reporter gene assay. The results revealed that miR‑138‑5p expression levels in patients with GBM from a Gene Expression Omnibus dataset were significantly downregulated. RT‑qPCR analysis of miR‑138‑5p expression levels also revealed similar results in GBM tissues and cell lines. The upregulation of miR‑138‑5p expression levels using a mimic significantly inhibited the cell viability, colony formation and the G0/G1 to S progression in GBM cell lines, suggesting that miR‑138‑5p may be a tumor suppressor. Moreover, miR‑138‑5p was discovered to directly target cyclin D3 (CCND3), a protein that serves an important role in the cell cycle, and inhibited its expression. Finally, silencing CCND3 using small interfering RNA suppressed the viability of GBM cells. In conclusion, the results of the present study suggested that miR‑138‑5p may function as a tumor suppressor in GBM by targeting CCND3, indicating that miR‑138‑5p may be a novel therapeutic target for patients with GBM.
View Figures
View References

Related Articles

Journal Cover

November-2020
Volume 20 Issue 5

Print ISSN: 1792-1074
Online ISSN:1792-1082

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Wu H, Wang C, Liu Y, Yang C, Liang X, Zhang X and Li X: miR‑138‑5p suppresses glioblastoma cell viability and leads to cell cycle arrest by targeting cyclin D3. Oncol Lett 20: 264, 2020
APA
Wu, H., Wang, C., Liu, Y., Yang, C., Liang, X., Zhang, X., & Li, X. (2020). miR‑138‑5p suppresses glioblastoma cell viability and leads to cell cycle arrest by targeting cyclin D3. Oncology Letters, 20, 264. https://doi.org/10.3892/ol.2020.12127
MLA
Wu, H., Wang, C., Liu, Y., Yang, C., Liang, X., Zhang, X., Li, X."miR‑138‑5p suppresses glioblastoma cell viability and leads to cell cycle arrest by targeting cyclin D3". Oncology Letters 20.5 (2020): 264.
Chicago
Wu, H., Wang, C., Liu, Y., Yang, C., Liang, X., Zhang, X., Li, X."miR‑138‑5p suppresses glioblastoma cell viability and leads to cell cycle arrest by targeting cyclin D3". Oncology Letters 20, no. 5 (2020): 264. https://doi.org/10.3892/ol.2020.12127