Interference of long non-coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR-26b-5p.

Ovarian cancer (OV) is the fifth most common type of cancer affecting women worldwide. Long non-coding RNAs (lncRNAs) serve essential roles in the progression of OV. As such, the present study aimed to investigate the specific role of HAGLR opposite strand lncRNA (HAGLROS) in OV and the underlying mechanism of action through which HAGLROS exerts its effects on OV cells. In the present study, the expression of HAGLROS in several OV cell lines was first detected using reverse transcription-quantitative PCR. HAGLROS was then silenced to evaluate cell viability, proliferation and apoptosis, which were determined using Cell Counting Kit-8, colony formation and TUNEL assays, respectively. Additionally, immunofluorescence staining and western blotting were used to confirm the expression profile of proliferation- and apoptosis-related proteins. Moreover, a dual luciferase reporter assay was used to verify the potential interactions between HAGLROS and microRNA (miR)-26b-5p. Subsequently, rescue assays were performed to investigate the effects of HAGLROS and miR-26b-5p on OV progression. The results indicated that HAGLROS was highly expressed in OV cells. Interference of HAGLROS led to a decrease in the proliferation, but an increase in the apoptosis of OV cells, accompanied by downregulated expression levels of Ki67 and Bcl-2, and upregulated expression levels of Bax and cleaved caspase-3. Further study revealed that HAGLROS acted as a sponge for miR-26b-5p and positively regulated its expression. miR-26b-5p inhibitor transfection partially reversed the effects of HAGLROS knockdown on the proliferation and apoptosis of OV cells. In conclusion, the results of the present study suggested that interference of HAGLROS suppressed the proliferation and promoted the apoptosis of OV cells through regulating miR-26b-5p, indicating that HAGLROS may be a promising biomarker in OV diagnosis and treatment.