Abstract
Nasopharyngeal carcinoma‑associated gene 6 (NGX6) is associated with the Wnt/β‑catenin signaling pathway in a number of different types of cancer, including colorectal cancer (CRC). The present study is aimed to determine the functional role of NGX6 in osteosarcoma (OS) and to investigate the underlying mechanism associated with the Wnt/β‑catenin signaling pathway. NGX6 expression levels in tissues derived from patients with OS and cell lines (MG‑63, Saos‑2, U2OS and HOS) was analyzed using reverse transcription‑quantitative PCR. NGX6 expression levels were subsequently overexpressed through transfection of the pcDNA3.1 (pcDNA)‑NGX6 overexpression vector into U2OS and HOS cells. BML284 was utilized to activate the Wnt/β‑catenin signaling pathway. MTT, wound healing, Transwell and flow cytometry assays were performed to analyze cell viability, migration, invasion and apoptosis, respectively. Western blotting was also used to analyze the protein expression levels of β‑catenin, c‑Jun and c‑Myc. A xenograft model was constructed by injecting pcDNA‑NGX6‑transfected U2OS cells into nude mice (BALB/c). The results of the present study revealed that the expression levels of NGX6 were downregulated in OS tissues and cell lines. The transfection of pcDNA‑NGX6 into OS cells significantly inhibited the cell viability, and migratory and invasive abilities, and induced the apoptosis of U2OS and HOS cells. The expression levels of β‑catenin, c‑Jun and c‑Myc were also significantly downregulated in pcDNA‑NGX6‑transfected U2OS and HOS cells. Notably, the treatment of transfected cells with BML284 significantly reversed the inhibitory effect of pcDNA‑NGX6 on the viability, migration and invasion, and the promoting effect on apoptosis in U2OS cells. Furthermore, NGX6 overexpression also discovered to inhibit the growth of xenograft tumors in vivo by inhibiting the Wnt/β‑catenin signaling pathway. In conclusion, the findings of the present study suggested that NGX6 may suppress the viability, migration and invasion, while facilitating the apoptosis of OS cells via blocking the Wnt/β‑catenin signaling pathway.