ArticleExperimental and therapeutic medicine2021
Interference of long non-coding RNA HAGLROS inhibits the proliferation and promotes the apoptosis of ovarian cancer cells by targeting miR-26b-5p.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Identification of lncRNAs Deregulated in Epithelial Ovarian Cancer Based on a Gene Expression Profiling Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- Mechanistic insights into HAGLROS-mediated therapy resistance in ovarian cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Review
- Article
- Mechanisms of apoptosis-related non-coding RNAs in ovarian cancer: a narrative review.Apoptosis : an international journal on programmed cell death · 2025Review
- A narrative review of papillary thyroid carcinoma-related long non-coding RNAs and their relevance to malignant tumors.Translational cancer research · 2025Review
- Competing endogenous RNA networks in ovarian cancer: from bench to bedside.EXCLI journal · 2025Review
- LncRNA HAGLROS: A Vital Oncogenic Propellant in Various Human Cancers.Current drug targets · 2025Review
- Deciphering the nexus between long non-coding RNAs and endoplasmic reticulum stress in hepatocellular carcinoma: biomarker discovery and therapeutic horizons.Cell death discovery · 2024Review
- LncRNA HAGLROS promotes breast cancer evolution through miR-135b-3p/COL10A1 axis and exosome-mediated macrophage M2 polarization.Cell death & disease · 2024Article
- 1,4,5,6,7,8‑Hexahydropyrido[4,3‑d]pyrimidine inhibits HepG2 cell proliferation, migration and invasion, and induces apoptosis through the upregulation of miR‑26b‑5p by targeting CDK8.Oncology letters · 2023Article
- The lncRNA PRINS-miRNA-mRNA Axis Gene Expression Profile as a Circulating Biomarker Panel in Psoriasis.Molecular diagnosis & therapy · 2022Article
- Article
- Long Noncoding RNA HAGLROS Promotes the Malignant Progression of Bladder Cancer by Regulating the miR-330-5p/SPRR1B Axis.Frontiers in oncology · 2022Article
- Long non-coding RNA HAGLROS promotes the development of diffuse large B-cell lymphoma via suppressing miR-100.Journal of clinical laboratory analysis · 2022Article
- Identification of Hub lncRNAs Along With lncRNA-miRNA-mRNA Network for Effective Diagnosis and Prognosis of Papillary Thyroid Cancer.Frontiers in pharmacology · 2021Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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