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Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin

Retraction in: /10.3892/ijmm.2024.5345
  • Authors:
    • Hua Yan
    • Bing‑Mei Sun
    • Yu‑Ying Zhang
    • Yu‑Juan Li
    • Cheng‑Xiang Huang
    • Fu‑Zhong Feng
    • Cui Li
  • View Affiliations / Copyright

    Affiliations: Department of Obstetrics and Gynecology, Linyi Central Hospital, Linyi, Shandong 276400, P.R. China
    Copyright: © Yan et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 2469-2480
    |
    Published online on: September 4, 2018
       https://doi.org/10.3892/ijmm.2018.3853
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Abstract

Endometrial cancer is a life‑threatening malignancy that affects women all over the world, and it has an increasing incidence. MicroRNAs (miRNAs/miRs) have been reported to be involved in cellular activities in endometrial cancer. The present study aimed to examine the effects of miR‑183‑5p on the epithelial‑mesenchymal transition (EMT), proliferation, invasion, migration and apoptosis of human endometrial cancer cells by targeting Ezrin. Primary endometrial cancer tissues and adjacent normal tissues were obtained for the investigation. The protein expression of Ezrin in tissues was detected by immunohistochemistry. The expression level of miR‑183‑5p and the mRNA and protein expression levels of Ezrin and EMT‑associated genes were determined by reverse transcription‑quantitative polymerase chain reaction and western blot analyses. Endometrial cancer cells were treated with miR‑183‑5p inhibitors, small interfering RNA targeting Ezrin or miR‑183‑5p inhibitors. Cell proliferation, cell cycle, apoptosis, migration and invasion were then evaluated using an MTT assay, flow cytometry, scratch test and Transwell assay, respectively. Compared with normal adjacent tissues, the expression of miR‑183‑5p was decreased in endometrial cancer tissues, and the expression of Ezrin was significantly increased in endometrial cancer tissues. The protein expression of Ezrin was correlated with the severity and poor prognosis of endometrial cancer. Notably, the target prediction program and the luciferase reporter gene assay confirmed that miR‑183‑5p targeted and negatively regulated the expression of Ezrin. In vivo experiments revealed that the increased expression of miR‑183‑5p and decreased expression of Ezrin inhibited EMT, cell proliferation, migration and invasion, but promoted cell apoptosis in Ishikawa cells. These results suggested that the upregulated expression of miR‑183‑5p promoted apoptosis and suppressed the EMT, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin.
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Copy and paste a formatted citation
Spandidos Publications style
Yan H, Sun BM, Zhang YY, Li YJ, Huang CX, Feng FZ and Li C: Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345. Int J Mol Med 42: 2469-2480, 2018.
APA
Yan, H., Sun, B., Zhang, Y., Li, Y., Huang, C., Feng, F., & Li, C. (2018). Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345. International Journal of Molecular Medicine, 42, 2469-2480. https://doi.org/10.3892/ijmm.2018.3853
MLA
Yan, H., Sun, B., Zhang, Y., Li, Y., Huang, C., Feng, F., Li, C."Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345". International Journal of Molecular Medicine 42.5 (2018): 2469-2480.
Chicago
Yan, H., Sun, B., Zhang, Y., Li, Y., Huang, C., Feng, F., Li, C."Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345". International Journal of Molecular Medicine 42, no. 5 (2018): 2469-2480. https://doi.org/10.3892/ijmm.2018.3853
Copy and paste a formatted citation
x
Spandidos Publications style
Yan H, Sun BM, Zhang YY, Li YJ, Huang CX, Feng FZ and Li C: Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345. Int J Mol Med 42: 2469-2480, 2018.
APA
Yan, H., Sun, B., Zhang, Y., Li, Y., Huang, C., Feng, F., & Li, C. (2018). Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345. International Journal of Molecular Medicine, 42, 2469-2480. https://doi.org/10.3892/ijmm.2018.3853
MLA
Yan, H., Sun, B., Zhang, Y., Li, Y., Huang, C., Feng, F., Li, C."Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345". International Journal of Molecular Medicine 42.5 (2018): 2469-2480.
Chicago
Yan, H., Sun, B., Zhang, Y., Li, Y., Huang, C., Feng, F., Li, C."Upregulation of miR-183-5p is responsible for the promotion of apoptosis and inhibition of the epithelial-mesenchymal transition, proliferation, invasion and migration of human endometrial cancer cells by downregulating Ezrin Retraction in /10.3892/ijmm.2024.5345". International Journal of Molecular Medicine 42, no. 5 (2018): 2469-2480. https://doi.org/10.3892/ijmm.2018.3853
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