Long non-coding RNA KCNQ1OT1 promotes ovarian cancer cell malignant characteristics by targeting the miR-140-5p/KLK10 axis.

Long non-coding RNAs (lncRNAs) have emerged as key regulatory molecules involved in driving cancer progression. However, the specific functional roles of numerous lncRNAs in ovarian cancer (OC) remain largely underexplored. The present study aimed to elucidate the role and underlying mechanisms of potassium voltage-gated channel subfamily Q member 1 opposite strand/antisense transcript 1 (KCNQ1OT1) in OC progression. Bioinformatics prediction using the TargetScan and starBase databases revealed that both KCNQ1OT1 and kallikrein-related peptidase 10 (KLK10) harbor complementary binding sites for microRNA (miR)-140-5p. The direct interaction between miR-140-5p and KCNQ1OT1 or KLK10 was experimentally validated using miRNA pull-down assays. Analysis of GEO datasets (GSE66957 and GSE47841), followed by RT-qPCR validation in SKOV3 and IOSE80 cells, revealed that KCNQ1OT1 and KLK10 were markedly upregulated, whereas miR-140-5p was downregulated in OC compared with that in normal ovarian controls. CCK-8 and wound-healing assays demonstrated that silencing KCNQ1OT1 markedly suppressed OC cell proliferation and migration, effects that were reversed by miR-140-5p inhibition. Conversely, inhibition of miR-140-5p enhanced OC cell proliferation and migration, which were abrogated by KLK10 knockdown. Collectively, these findings identified a previously unrecognized regulatory axis in OC, in which KCNQ1OT1 promotes tumor cell proliferation and migration by modulating the miR-140-5p/KLK10 pathway. The present study advances the mechanistic understanding of lncRNA-mediated oncogenesis and provides preliminary evidence supporting a potential role of KCNQ1OT1 in OC progression.