Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Role of MiR-205/PTEN in cisplatin-resistant esophageal squamous cell carcinoma

Xun Tang^1-3, Xuelian Mao^1-3, Feng Yan^1-3

¹Jiangsu Cancer Hospital; ²Jiangsu Institute of Cancer Research; ³Department of Clinical Laboratory, The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, 210009, China.

For correspondence:- Feng Yan Email: yanfengjiop@163.com

Accepted: 26 November 2018 Published: 26 December 2018

Citation: Tang X, Mao X, Yan F. Role of MiR-205/PTEN in cisplatin-resistant esophageal squamous cell carcinoma. Trop J Pharm Res 2018; 17(12):2347-2353 doi: 10.4314/tjpr.v17i12.5

© 2018 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 evaluate the effect of miRNA-205 on cisplatin-resistant TE13 cell lines, and the interaction of miRNA-205 with downstream signaling pathway.

Methods: TE13 cells were treated with cisplatin at a concentration of 1.5 μg/mL every 24 h for 3 months. Cisplatin-resistant cell lines were maintained in the continuous presence of 2 μg/ml cisplatin and supplemented every 72 h. Half-maximal inhibitory concentration (IC₅₀) value was determined by MTT assay, and cell apoptosis was tested by flow cytometry. In addition, luciferase reporter assay was conducted to test the binding of miRNA-205 and phosphatase and tensin homologue deleted on chromosome 10 (PTEN) 3’UTR.

Results: The cisplatin-resistant (cis-TE13) cell line was well established based on IC₅₀ values (cis-TE13, IC₅₀ = 2.215; TE13, IC₅₀ = 0.304). The levels of miRNA-205, phosphatase, PTEN, and protein kinase B (p-AKT) were abnormally expressed in cis-TE13 cells. Overexpression of miRNA-205 significantly promoted cell viability and decreased cell apoptosis of cis-TE13 cells as indicated by IC₅₀ values (cis-TE13, IC₅₀ = 3.537; TE13, IC₅₀ = 0.580). Moreover, miRNA-205 significantly activated p-AKT expression by inhibiting PTEN expression. In contrast to miRNA-205, PTEN overexpression inhibited cell viability, increased cell apoptosis of cis-TE13 cells (cis-TE13, IC₅₀ = 2.625; TE13, IC₅₀ = 0.246), decreased the expression of p-AKT, and counteracted the regulation of miRNA-205 (control, IC₅₀ = 2.297; miR-205, IC₅₀ = 4.693; miR-205+PTEN, IC₅₀ = 2.011).

Conclusion: These findings indicate that miRNA-205 exacerbates esophageal squamous cell carcinoma via inhibition of PTEN expression, suggesting the potential value of miRNA-205 in the diagnosis or treatment of esophageal squamous cell carcinoma.

Keywords: miRNA-205, PTEN, PI3K/AKT signaling pathway, Esophageal squamous cell, Carcinoma, Cisplatin resistance