LncRNA SOX9-AS1 promotes the development of endometrial cancer by sponging miR-497-5p and upregulating E2F transcription factor 3.

Abstract

Endometrial cancer (EC) is one of the most prevalent gynecologic malignancies, and long non-coding RNA (lncRNA) SOX9-AS1 has been identified as being upregulated in various cancers, indicating its potential role in driving carcinogenesis. However, the involvement and mechanism of SOX9-AS1 in EC have not been thoroughly investigated. The expression of SOX9-AS1 was assessed using qRT-PCR. The impact of molecular intervention on EC cells was evaluated through cell viability, migration, and invasion assays. Survival probability was analyzed using the Kaplan-Meier method. Bioinformatics predictions, dual-luciferase reporter assays, and rescue experiments were conducted to elucidate the specific competitive endogenous RNA (ceRNA) mechanism of the SOX9-AS1/miR-497-5p/E2F3 axis. SOX9-AS1 expression was significantly upregulated in EC tissues and cells, correlating with poor prognosis in EC patients. Knockdown of SOX9-AS1 inhibited the proliferation, migration, invasion, and glycolysis of EC cells. Mechanistically, miR-497-5p suppressed the proliferation, migration, invasion, and glycolysis of EC by targeting E2F3. Molecular interaction analysis indicate that SOX9-AS1 functions as a molecular sponge for miR-497-5p, thereby increasing E2F3 expression. Our work unveiled a novel mechanism by which SOX9-AS1 promotes EC development, suggesting that targeting the SOX9-AS1/miR-497-5p/E2F3 axis may represent a potential therapeutic strategy for EC.