ArticleJournal of clinical laboratory analysis2022
HAGLROS knockdown restrained cell proliferation, migration and invasion and facilitated apoptosis in laryngeal cancer via miR-138-5p/CLN5 axis.
Article in Journal of clinical laboratory analysis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- MiR-138-5p Suppresses Glucose Metabolism to Inhibit the Progression of Nasopharyngeal Carcinoma by Targeting the CENPN/PI3K/Akt/mTOR Signaling.Journal of biochemical and molecular toxicology · 2026Article
- A narrative review of papillary thyroid carcinoma-related long non-coding RNAs and their relevance to malignant tumors.Translational cancer research · 2025Review
- LncRNA HAGLROS: A Vital Oncogenic Propellant in Various Human Cancers.Current drug targets · 2025Review
- The Role of miR-138 in Cardiovascular Diseases.BioMed research international · 2025Review
- HAGLROS knockdown restrained cell proliferation, migration and invasion and facilitated apoptosis in laryngeal cancer via miR-138-5p/CLN5 axis.Journal of clinical laboratory analysis · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundThis work investigated the role of HAGLROS in laryngeal cancer (LC).
methodsHAGLROS expression in the head and neck squamous cell carcinoma (HNSC), target miRNAs of HAGLROS, target mRNAs of miR-138-5p, and the binding sites of HAGLROS and miR-138-5p or CLN5 and miR-138-5p were predicted through bioinformatics. HAGLROS, miR-138-5p, CLN5, Bcl-2, and Bax levels were detected by qRT-PCR and Western blot. The biological functions of LC cells were assessed through CCK-8, colony formation assays, transwell assay, and flow cytometry assay. The targeting relationship between HAGLROS and miR-138-5p or CLN5 and miR-138-5p was confirmed by dual luciferase gene reporter analysis.
resultsHAGLROS was upregulated in LC. HAGLROS-specific small interfering RNA (Si-HAGLROS) inhibited the viability, proliferation, migration, and invasion while increased the apoptosis in LC cells. MiR-138-5p was a target of HAGLROS and the miR-138-5p inhibitor reversed the effects of si-HAGLROS on LC cells. CLN5 was a target of miR-138-5p. MiR-138-5p inhibitor raised the viability, migration and invasion, and Bcl-2 expression while declined Bax expression in LC cells, with si-CLN5 performing the opposite effects and reversing the effects of miR-138-5p inhibitor.
conclusionSilenced HAGLROS restrained the LC cells' abilities to proliferate, migrate, and invade as well as facilitated apoptosis in LC via miR-138-5p/CLN5 axis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.