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

Abstract

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.

The lncRNA PRINS-miRNA-mRNA Axis Gene Expression Profile as a Circulating Biomarker Panel in Psoriasis

“…Gene ontology of the PRINS lncRNA-miRNA-mRNA under study revealed that the axis is functioning mainly in the regulation of cytokine production involved in the inflammatory response, gene silencing by miRNA, and regulation of gene expression, data in line with previous studies [37,[44][45][46][47][48][49][50][51][52][53][54][55]. The biological functions are correlated with the molecular function as the LncRNA-miRNA-mRNA under study are involved in gene silencing at both the transcriptional and post-transcriptional levels by binding to transcription factor, TAT protein (a regulator of gene expression), mRNA 3′-untranslated region, and large and small ribosomal subunits .…”

Long Noncoding RNA HAGLROS Promotes the Malignant Progression of Bladder Cancer by Regulating the miR-330-5p/SPRR1B Axis

“…Lin et al. reported that knockdown HAGLROS can suppress the proliferation and promote the apoptosis of ovarian cancer cells by regulating miR-26b-5p, which affects the expression of apoptosis-related proteins ( 24 ). Notably, recent study indicated that HAGLROS was highly expressed and decreasing HAGLROS can inactivate the mTOR axis and elevate autophagy through improving lipid metabolism reprogramming in intrahepatic cholangiocarcinoma ( 25 ).…”

Long non-coding RNA HAGLROS facilitates tumorigenesis and progression in hepatocellular carcinoma by sponging miR-26b-5p to up-regulate karyopherin α2 (KPNA2) and inactivate p53 signaling

“…That is to say, HAGLROS could exert tumor-promoting role in HCC by sponging miR-26b-5p. A similar document found that interference of HAGLROS repressed the proliferation and induced the apoptosis of ovarian cancer cells by targeting miR-26b-5p [ 38 ]. However, the effects of HAGLROS on cell migration and invasion, and tumor growth were not investigated.…”