Open Access

miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2

Retraction in: /10.3892/etm.2021.10883

  • Authors:
    • Shaoqiang Liang
    • Ning Zhang
    • Yanming Deng
    • Lusi Chen
    • Yang Zhang
    • Zhenhe Zheng
    • Weijun Luo
    • Zhiqian Lv
    • Shaoen Li
    • Tao Xu
  • View Affiliations

  • Published online on: June 14, 2017     https://doi.org/10.3892/etm.2017.4608
  • Pages: 1095-1103
  • Copyright: © Liang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The authors' previous study revealed that the serum levels of microRNA (miR)-663b are significantly increased in patients with nasopharyngeal carcinoma (NPC), and are associated with NPC progression and poor prognosis. However, the molecular mechanism of underlying NPC growth and metastasis remains unclear. In the present study, quantitative polymerase chain reaction and western blot analyses were performed to examine changes to mRNA and protein expression, respectively. MTT, wound healing and Transwell assays were used to examine cell proliferation, migration and invasion, respectively. Luciferase reporter gene assays were performed to identify target genes of miR‑663b. It was demonstrated that miR‑663b was significantly upregulated in NPC tissue compared with non‑tumor nasopharyngeal epithelial tissue samples. Furthermore, miR‑663b expression gradually increased with advancing stages of NPC, with the highest expression being observed in the latest stage IV. The increased expression of miR‑663b was associated with advanced clinical stage and lymph node metastasis. In addition, miR‑663b expression was increased in NPC cell lines compared with normal nasopharyngeal epithelial NP69 cells. Knockdown of miR‑663b resulted in a significant reduction in the proliferation, migration and invasion of NPC CNE1 cells. Tumor suppressor candidate 2 (TUSC2) was identified as a novel target gene of miR‑663b. It was further demonstrated that TUSC2 was significantly downregulated in NPC tissue samples and cell lines. miR‑663b negatively regulated the expression of TUSC2 at the post‑transcriptional level in CNE1 cells. Additionally, inhibition of TUSC2 expression attenuated the suppressive effects of miR‑663b downregulation on the proliferation, migration and invasion of CNE1 cells. To the best of our knowledge, this is the first study to demonstrate that miR‑663b, which is upregulated in NPC, promotes the proliferation, migration and invasion of NPC cells, partially through the inhibition of TUSC2 expression. Therefore, it is suggested that miR‑663b is a promising therapeutic target for the treatment of patients with NPC.
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August-2017
Volume 14 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Liang S, Zhang N, Deng Y, Chen L, Zhang Y, Zheng Z, Luo W, Lv Z, Li S, Xu T, Xu T, et al: miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2 Retraction in /10.3892/etm.2021.10883. Exp Ther Med 14: 1095-1103, 2017.
APA
Liang, S., Zhang, N., Deng, Y., Chen, L., Zhang, Y., Zheng, Z. ... Xu, T. (2017). miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2 Retraction in /10.3892/etm.2021.10883. Experimental and Therapeutic Medicine, 14, 1095-1103. https://doi.org/10.3892/etm.2017.4608
MLA
Liang, S., Zhang, N., Deng, Y., Chen, L., Zhang, Y., Zheng, Z., Luo, W., Lv, Z., Li, S., Xu, T."miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2 Retraction in /10.3892/etm.2021.10883". Experimental and Therapeutic Medicine 14.2 (2017): 1095-1103.
Chicago
Liang, S., Zhang, N., Deng, Y., Chen, L., Zhang, Y., Zheng, Z., Luo, W., Lv, Z., Li, S., Xu, T."miR-663b promotes tumor cell proliferation, migration and invasion in nasopharyngeal carcinoma through targeting TUSC2 Retraction in /10.3892/etm.2021.10883". Experimental and Therapeutic Medicine 14, no. 2 (2017): 1095-1103. https://doi.org/10.3892/etm.2017.4608