Long non-coding RNA SNHG9 inhibits ovarian cancer progression by sponging microRNA-214-5p.

Ovarian cancer ranks 7th among the most common cancer types affecting women worldwide. A number of studies have confirmed that multiple long non-coding RNAs participate in the occurrence and progression of ovarian cancer. Small nucleolar RNA host gene 9 (SNHG9) serves a role in the progression of glioblastoma and pancreatic cancer. However, the specific biological function of SNHG9 in ovarian cancer has not yet been fully investigated. The present study aimed to determine the biological role and potential molecular mechanism underlying the influence of SNHG9 in ovarian cancer. SNHG9 expression in ovarian cancer cell lines and tissues were measured via reverse transcription-quantitative PCR analysis, and cell proliferation was detected via Cell Counting Kit-8 and colony formation assays. Flow cytometry was performed to assess cell cycle progression, and Transwell and wound healing assays were performed to assess cell invasion and migration abilities. Bioinformatics software was utilized to determine the target genes of SNHG9, which were subsequently verified via dual-luciferase reporter and RNA immunoprecipitation assays. The results demonstrated that SNHG9 expression was remarkably lower in ovarian cancer cell lines and tissues compared with the negative controls. Cell function assays demonstrated that decreased SNHG9 expression notably induced the migration, colony formation, proliferation and invasiveness of ovarian cancer cells. Furthermore, the inhibitory effect of SNHG9 on the migration, colony formation, proliferation and invasion of ovarian cancer cells was partially reversed by miR-214-5p upregulation. Thus, taken together, the current results suggest that SNHG9 may serve as a tumor suppressor gene in ovarian cancer by regulating the miR-214-5p/cryptochrome circadian regulator 2 axis.