LncRNA SNHG29 Suppresses Epithelial Ovarian Cancer Cell Invasion and Migration via miR-20b-3p/GNAI3 Axis Regulation

Epithelial ovarian cancer (EOC) is the deadliest gynecologic cancer in women. Long noncoding RNAs (lncRNAs) are critically involved in malignant progression by modulating proliferation, apoptosis, invasion, metastasis, and chemotherapy resistance. The long noncoding RNA small nucleolar RNA host gene 29 (SNHG29) is involved in multiple malignancies, although its role in EOC has not been elucidated. In our study, SNHG29 expression was significantly downregulated in EOC tissues and was negatively related to lymphatic invasion in EOC patients according to data from the TCGA database. Kaplan-Meier survival analysis revealed that among patients with early stage EOC, compared with patients with low SNHG29 expression levels, patients with high expression levels had markedly longer progression-free survival (PFS) and overall survival (OS) times. Further studies suggested that SNHG29 knockdown enhanced the invasive and migrative potential of EOC cells, whereas SNHG29 overexpression attenuated the invasive and migrative potential capacity. In animal experiments, SNHG29 knockdown significantly promoted lung metastasis in tail vein injection models. Mechanistically, the downregulation of SNHG29 expression inhibited its competitive endogenous RNA activity, resulting in increased miR-20b-3p availability and subsequent degradation of the downstream target gene GNAI3, as determined by RNA immunoprecipitation (RIP) and luciferase reporter gene assays. miR-20b-3p inhibition significantly reduces the invasive and metastatic capabilities of EOC cells resulting from a reduction in SNHG29 expression. Our study revealed that SNHG29 may be a promising prognostic factor and therapeutic target for EOC.