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

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.