H3K27ac-activated lncRNA KTN1-AS1 aggravates tumor progression by miR-505-3p/ZNF326 axis in ovarian cancer

Background: Numerous studies indicate that long noncoding RNA (lncRNA) is aberrantly expressed in ovarian cancer (OC). Our research investigated the regulatory role of lncRNA KTN1 antisense RNA1 (KTN1-AS1) in the progression of OC through the miR-505-3p/ZNF326 axis.

Methods: Expression of KTN1-AS1, microRNA-505-3p (miR-505-3p), and zinc-finger protein-326 (ZNF326) in OC was evaluated by using RT-qPCR analysis. The biological function of KTN1-AS1 was inspected using the loss-of-function assay. Luciferase reporter assay and RIP assay were performed to determine the competitive endogenous RNA (ceRNA) network of KTN1-AS1/miR-505-3p/ZNF326.

Results: The data showed that KTN1-AS1 and ZNF326 had a high expression in OC than in the normal tissue, and miR-505-3p exhibited a low expression in OC than in the normal tissue. The knockdown of KTN1-AS1 caused an inhibition in OC cell proliferation, migration, and invasion, and promoted cell apoptosis. In terms of mechanical exploration, KTN1-AS1 was transcriptionally activated by histone H3 on lysine 27 acetylation (H3K27ac) at the promoter region, and KTN1-AS1 increased ZNF326 expression by competitively adsorbing miR-505-3p.

Conclusions: This study indicated that H3K27ac-induced lncRNA KTN1-AS1 expression, and facilitated proliferation, migration, and invasion of OC cells by the KTN1-AS1/miR-505-3p/ZNF326 axis.