ArticleCancer biomarkers : section A of Disease markers2020
HOTAIR inhibits the proliferation of glioblastoma cells by targeting miR-219.
Article in Cancer biomarkers : section A of Disease markers, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 9 citations in OpenAlex.
- MicroRNA-219 in the central nervous system: a potential theranostic approach.Research in pharmaceutical sciences · 2024Review
- Roles of HOTAIR Long Non-coding RNA in Gliomas and Other CNS Disorders.Cellular and molecular neurobiology · 2024Review
- Study of lncRNAs in Pediatric Neurological Diseases: Methods, Analysis of the State-of-Art and Possible Therapeutic Implications.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Novel sights on therapeutic, prognostic, and diagnostics aspects of non-coding RNAs in glioblastoma multiforme.Metabolic brain disease · 2023Review
- Noncoding RNAs in pediatric brain tumors: Molecular functions and pathological implications.Molecular therapy. Nucleic acids · 2021Review
- The Role of lncRNAs in Rare Tumors with a Focus on HOX Transcript Antisense RNA (International journal of molecular sciences · 2021Review
- Long Non-Coding RNAs in Diagnosis, Treatment, Prognosis, and Progression of Glioma: A State-of-the-Art Review.Frontiers in oncology · 2021Review
- Critical role of HOX transcript antisense intergenic RNA (HOTAIR) in gliomas.Journal of molecular medicine (Berlin, Germany) · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTo investigate the influences of HOX transcript antisense ribonucleic acid (HOTAIR) on the proliferation and apoptosis of glioblastoma cells by targeting micro RNA (miR)-219.
objectiveWith glioblastoma cell line U87 as the object, the changes in expression levels of HOTAIR and miR-219 in each group were detected via quantitative real-time polymerase chain reaction (qRT-PCR) after HOTAIR in U87 cell lines was knocked down using small interfering RNA (siRNA). Then the cell proliferation in each group was determined using Cell Counting Kit-8 (CCK-8) and colony formation assays. Flow cytometry was applied to detect the cell apoptosis, and Western blotting assay was adopted to measure the changes in protein levels of Cyclin D1 and Bcl-2-associated X protein (Bax). After miR-219 knockdown with siRNA, the changes in expression levels of HOTAIR and miR-219 in each group were examined through qRT-PCR, and the cell proliferation was tested by CCK-8 assay.
resultsAfter interference inHOTAIR using siRNA, compared with those in control group, the RNA expression level of HOTAIR was decreased remarkably (p< 0.05), the RNA expression level of miR-219 was increased notably (p< 0.05), the cell proliferation rate was inhibited evidently (p< 0.05), the apoptosis rate was enhanced obviously (p< 0.05), the protein expression level of Cyclin D1 declined markedly (p< 0.05), and the protein expression level of Bax rose distinctly (p< 0.05) in HOTAIR-siRNA group. After miR-219 knockdown with siRNA, the cell proliferation rate was raised remarkably (p< 0.05), but there was no significant change in the RNA expression level of HOTAIR (p> 0.05).
conclusionHOTAIR can repress the proliferation and promote the apoptosis of glioblastoma cells by targeting miR-219.
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