Open Access

MicroRNA‑195 inhibits epithelial‑mesenchymal transition by targeting G protein‑coupled estrogen receptor 1 in endometrial carcinoma

  • Authors:
    • Junfeng Deng
    • Weihua Wang
    • Guangyu Yu
    • Xiuzhen Ma
  • View Affiliations

  • Published online on: September 6, 2019     https://doi.org/10.3892/mmr.2019.10652
  • Pages: 4023-4032
  • Copyright: © Deng 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

Epithelial‑mesenchymal transition (EMT) has been shown to exert promoting effects on the progression of a number of cancer types, including endometrial carcinoma (EC). MicroRNA (miRNA or miR)‑195 has been shown to function as a tumor suppressor. This study aimed to explore the potential role of miR‑195 in the EMT process of EC. miR‑195 overexpression (Mimics) and mimics control (Mock) vectors were constructed and transfected into human endometrial cancer cells (AN3‑CA and Hec1A) using Lipofectamine 2000, and cell viability was detected using the Cell Counting kit‑8 (CCK‑8). The invasive and migratory capacities of the cells transfected with the Mimics or Mock vectors were assessed by Transwell and wound healing assays. Relative mRNA and protein levels were analyzed by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) and western blot analysis, respectively. Using TargetScan prediction, the potential target of miR‑195 was identified and was further verified by dual‑luciferase reporter assay. Following transfection with miR‑195 mimics, the viability of the AN3‑CA and Hec1A cells decreased in a time‑dependent manner, specifically at 24 h. The wound closure rate and the number of invaded cells in the Mimics group were much lower than those in the Control and Mock groups (P<0.01). miR‑195 overexpression significantly upregulated the mRNA and protein levels of tissue inhibitor of metalloproteinase 2 (TIMP‑2), while it downregulated the expression levels of matrix metalloproteinase (MMP)‑2 and MMP‑9. Moreover, the phosphorylation levels of PI3K and AKT were also notably decreased (P<0.01). G protein‑coupled estrogen receptor 1 (GPER) was identified as a target of miR‑195. On the whole, the findings of this study indicate that the inhibitory effects of miR195 on EC cell migration and invasion are associated with the PI3K/AKT signaling pathway and GPER expression.
View Figures
View References

Related Articles

Journal Cover

November-2019
Volume 20 Issue 5

Print ISSN: 1791-2997
Online ISSN:1791-3004

Sign up for eToc alerts

Recommend to Library

Copy and paste a formatted citation
x
Spandidos Publications style
Deng J, Wang W, Yu G and Ma X: MicroRNA‑195 inhibits epithelial‑mesenchymal transition by targeting G protein‑coupled estrogen receptor 1 in endometrial carcinoma. Mol Med Rep 20: 4023-4032, 2019
APA
Deng, J., Wang, W., Yu, G., & Ma, X. (2019). MicroRNA‑195 inhibits epithelial‑mesenchymal transition by targeting G protein‑coupled estrogen receptor 1 in endometrial carcinoma. Molecular Medicine Reports, 20, 4023-4032. https://doi.org/10.3892/mmr.2019.10652
MLA
Deng, J., Wang, W., Yu, G., Ma, X."MicroRNA‑195 inhibits epithelial‑mesenchymal transition by targeting G protein‑coupled estrogen receptor 1 in endometrial carcinoma". Molecular Medicine Reports 20.5 (2019): 4023-4032.
Chicago
Deng, J., Wang, W., Yu, G., Ma, X."MicroRNA‑195 inhibits epithelial‑mesenchymal transition by targeting G protein‑coupled estrogen receptor 1 in endometrial carcinoma". Molecular Medicine Reports 20, no. 5 (2019): 4023-4032. https://doi.org/10.3892/mmr.2019.10652