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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 LNATM 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.

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