lncRNA SNHG8 promotes aggressive behaviors of nasopharyngeal carcinoma via regulating miR-656-3p/SATB1 axis.

• Increased SNHG8 expression in nasopharyngeal carcinoma. • SNHG8 promotes nasopharyngeal carcinoma progression in vitro and in vivo. • miR-656−3p/SATB1 was the effector molecules of SNHG8. Long non-coding RNA (lncRNA) has been proposed to regulate tumorigenesis, however, the role of small nucleolar RNA host gene 8 (SNHG8) in nasopharyngeal carcinoma (NPC) remains unclear. Levels of SNHG8 in NPC tissues and cells were analyzed with real‐time quantitative PCR method. Cell counting kit-8 assay, colony formation assay, wound-healing assay, and transwell invasion assay were performed to detect cell viability, migration, and invasion. Luciferase activity assay and RIP assay were performed to explore relationships among SNHG8, microRNA-656−3p (miR-656−3p), and special AT-rich sequence-binding protein 1 (SATB1). We found SNHG8 level was increased expression in NPC tissues and cells. In vitro assays revealed that SNHG8 stimulates NPC cell proliferation, colony formation, cell migration, and cell invasion. In vivo assay confirmed knockdown of SNHG8 could hamper tumor growth. Furthermore, we showed SNHG8 serves as a sponge for miR-656−3p to regulate SATB1 expression, and participated in NPC progression. In summary, our work indicated the importance of SNHG8 in NPC progression, which provided novel treatment methods for NPC. [ABSTRACT FROM AUTHOR]