The emerging evidence showed that lncRNAs (long non-coding RNAs) could regulate the progression and affect the malignant behaviors of cancers. LncRNA SNHG8 (small nucleolar RNA host gene 8) has been reported to participate in most cancers development. Here in this study, the role of lncRNA SNHG8 in esophageal cancer was uncovered by a series of functional experiments. The expression pattern of SNHG8 in tumor tissues or cells was first detected by qRT-PCR. Using a lentivirus knockdown shRNA is to repress the expression of SNHG8. Subsequently, the in vitro and in vivo experiments were utilized to evaluate whether the malignant behaviors of esophageal cancer were influenced by knockdown SNHG8. The results indicated that lncRNA SNHG8 should be a cancer-promoting factor with a relatively high expression level in esophageal cancer. Moreover, knockdown SNHG8 inhibited the cell viability and induced cell apoptosis in KYSE30 and TE-1 cells. In addition, based on the results of the binding site analysis and the luciferase reporter system, SNHG8 functions by the miR-1270/BACH1 axis. The follow-up experiments verified that lncRNA SNHG8 could down-regulate the expression of miR-1270 to increase the BACH1 expression. Finally, we confirmed that knockdown SNHG8 retarded the progression of esophageal cancer with a xenograft model. To sum up, our findings suggested that lncRNA SNHG8 is a cancer-promoting factor in esophageal cancer. Knockdown SNHG8 could suppress the progression of esophageal cancer, which implies SNHG8 could be used as a therapeutic target in esophageal cancer.
Keywords: BACH1; SNHG8; esophageal cancer; lncRNA; miR-1270.