Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Effect of dexmedetomidine on miR-144-3p expression and epithelial mesenchymal transition in gastric cancer cells

Zong Chen¹, Yong Ding¹, Ying Zeng², Zhifeng Chen¹, Xueping Zhang³, Jianyan Chen^1,2

¹Department of Anesthesiology, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou; China; ²Department of Anesthesiology, Shenzhen Hospital of integrated traditional Chinese and Western Medicine, Shenzhen, China; ³Department of Anesthesiology, Shenzhen People's Hospital, The Second Clinical Medical College, Jinan University, Shenzhen Anesthesiology Engineering Center, Shenzhen 518020, China.

For correspondence:- Jianyan Chen Email: yan19o@163.com

Accepted: 6 October 2021 Published: 30 November 2021

Citation: Chen Z, Ding Y, Zeng Y, Chen Z, Zhang X, Chen J. Effect of dexmedetomidine on miR-144-3p expression and epithelial mesenchymal transition in gastric cancer cells. Trop J Pharm Res 2021; 20(11):2249-2253 doi: 10.4314/tjpr.v20i11.2

© 2021 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To investigate the effect of dexmedetomidine (DEX) on epithelial mesenchymal transition (EMT) in gastric cancer cells, and the role of microRNA-144-3p (miR-144-3p) in the process.

Methods: The effect of DEX on miRNA expression profile was analyzed using GEO database (https://www.ncbi.nlm.nih.gov/gds/). Human gastric cancer cells were cultured in vitro, and one group of cells was treated with saline for 48 h (control group). Cells treated with DEX at doses of 0.01, 0.1 and 1.0 μmol/L for 48 h were marked as low-, medium- and high-DEX concentration groups. The mRNA expression levels of miR-144-3p, ZEB1, E-cadherin and vimentin were determined using real-time quantitative polymerase chain reaction (RT-PCR), while the protein expressions of ZEB1, E-cadherin and vimentin were assayed with Western blotting. Cell proliferation was determined with CCK-8 assay, while metastasis was measured using Transwell assay.

Results: The GEO database demonstrated that the expression of miR-144-3p in rat cardiomyocytes was significantly decreased after DEX treatment (p < 0.05). The expression of miR-144-3p was decreased in all groups, when compared to the control group, but the expressions of ZEB1 and vimentin were increased, while that of E-cadherin was down-regulated (p < 0.05). Cell proliferation in the high-DEX concentration group was decreased (p < 0.05). The degrees of cell invasion and migration were increased in the medium- and high-DEX concentration groups (p < 0.05).

Conclusion: DEX promotes the metastasis of gastric cancer cells by regulation of epithelial mesenchymal transition (EMT) and the expression of miR-144-3p. This finding provides a new insight into the treatment of gastric cancer.

Keywords: Gastric cancer, Dexmedetomidine, E-cadherin, Vimentin, MiR-144-3p, Tumor metastasis, Epithelial mesenchymal transition