MicroRNA‑19b inhibitors can attenuate the STAT3 signaling pathway in NPC C666‑1 cells.

Abstract

MicroRNA (miR)-19b is expressed in various types of tumors and may serve as a potential therapeutic target. The miR-17-92 cluster is upregulated in nasopharyngeal carcinoma (NPC) tissues and cells. miR-19b is a member of the miR-17-92 cluster; however, its expression and function in NPC are largely unknown. The present study aimed to investigate the expression and function of miR-19b in NPC cells. The miRCURY LNA™ miRNA Inhibitor (miR-19b inhibitor and negative control) were transfected into C666-1 cells. The proliferation, apoptosis and migration of the cells were subsequently detected by the Cell Counting Kit-8 assay, flow cytometry and Transwell assay, respectively. Additionally, the expression of STAT3 signaling pathway-associated proteins [STAT3, pSTAT3 and suppressor of cytokine signaling 1 (SOCS1)] and the transcriptional targets of pSTAT3 [Bcl-2, myeloid leukemia protein 1 (Mcl-1) and cyclin D1] were detected by western blotting. The miR-19b inhibitor inhibited proliferation and migration and induced apoptosis of C666-1 cells. Furthermore, the miR-19b inhibitor upregulated the expression of SOCS1, a predicted target gene of miR-19b, and decreased the phosphorylation of STAT3 at Tyr705 and Ser727. These data indicated that upregulation of SOCS1, an endogenous inhibitor of STAT3 phosphorylation, attenuated the STAT3 signaling pathway in C666-1 cells. Moreover, the expression level of the proproliferative protein cyclin D1 and antiapoptotic proteins Mcl-1 and Bcl-2 was significantly decreased following transfection with the miR-19b inhibitor. The aforementioned three proteins are downstream transcriptional targets of the activated STAT3 signaling pathway. The results of the present study revealed that inhibition of miR-19b negatively modulated the malignant behavior of NPC cells via the STAT3 signaling pathway. Therefore, miR-19b inhibition may serve as a novel therapeutic target for the treatment of NPC.