The efficacy of cisplatin on nasopharyngeal carcinoma cells may be increased via the downregulation of fibroblast growth factor receptor 2.

Abstract

Cisplatin is one of the primary compounds used in the treatment of nasopharyngeal carcinoma (NPC), and fibroblast growth factor receptor 2 (FGFR2) has emerged to be a promising target for treatment in various tumors. Therefore, the present study aimed to explore whether the expression levels of FGFR2 in NPC tissues and cell lines were altered, and whether the efficiency of cisplatin was increased following the downregulation of FGFR2. The downregulation of FGFR2 was achieved by transfection with a small interfering RNA against FGFR2. Tissues of patients with NPC were analyzed by immunohistochemistry. Cell viability was examined using a Cell Counting Kit-8 assay. Cell cycle analysis was performed using flow cytometry. mRNA and protein levels were measured by reverse transcription quantitative polymerase chain reaction and western blot analysis, respectively. FGFR2 was observed to be overexpressed in cancer tissues of patients with NPC and in the NPC SUNE1, C666-1, 6-10B and HNE-3 cell lines, and resulted in an unfavorable prognosis. Cisplatin treatment decreased cell viability and increased FGFR2 expression. The silencing of FGFR2 was demonstrated to augment the effects of cisplatin treatment, including decreasing the cell viability and inducing cell cycle arrest, which involved the increase and decrease of the durations of G1 and S phases, respectively, and a decrease in the expression levels of cyclin D1 and CDC25A, and increasing the rate of apoptosis via the intrinsic apoptosis pathway, as demonstrated by the upregulation of cleaved caspase-3 and B-cell lymphoma 2 (Bcl-2)-associated X protein and downregulation of Bcl-2, in SUNE1 and C666-1 cell lines. FGFR2 was overexpressed in the cancer tissues of patients with NPC and in NPC cell lines, resulting in an unfavorable prognosis. The downregulation of FGFR2 decreased cell viability via cell cycle arrest at G1 phase, and increased the efficacy of the cisplatin-based induction of apoptosis through the intrinsic apoptosis pathway.