ArticleAging2023
LncRNA HAGLROS contribute to papillary thyroid cancer progression by modulating miR-206/HMGA2 expression.
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- The Intricate Interplay of Noncoding RNAs and the Gut Microbiome in Gastrointestinal and Endocrine-Related Cancers.Sub-cellular biochemistry · 2026Review
- LncRNA HOTAIR promotes cell proliferation and migration in papillary thyroid carcinoma cells by sponging miR-206/c-Met axis.Journal of molecular histology · 2025Article
- Modulation of RASD2 by miRNA-485-5p Drives Thyroid Cancer Progression and Metastasis.The Kaohsiung journal of medical sciences · 2025Article
- Dual roles of long non-coding RNAs in thyroid cancer: regulation of programmed cell death pathways.Medical oncology (Northwood, London, England) · 2025Review
- A narrative review of papillary thyroid carcinoma-related long non-coding RNAs and their relevance to malignant tumors.Translational cancer research · 2025Review
- lncRNA ACVR2B-AS1 modulates thyroid cancer progression by regulating miR-195-5p.Discover oncology · 2025Article
- LncRNA HAGLROS: A Vital Oncogenic Propellant in Various Human Cancers.Current drug targets · 2025Review
- Expression of CLDN1 and EGFR in PTC.Discover oncology · 2024Article
- Novel role of lncRNAs regulatory network in papillary thyroid cancer.Biochemistry and biophysics reports · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePapillary thyroid cancer (PTC) is one of the most serious diseases of the endocrine system. In view of the limited therapeutic effects of current medical methods, this study starts from the molecular level and looks for potential treatments. The interaction between HAGLROS/miR-206/HMGA2 was studied using multi-omics methods, which provided new ideas and methods for future treatments.
methodMicroarray analysis and R language were used for differential analysis to screening experimental targets of lncRNA, miRNA, and mRNA. qRT-PCR was used to detect RNA expression in tissues and cells. Double luciferase reporter assays analyzed and validated binding relationships between different RNAs. Colony formation, flow cytometry, and transwell assays were used to measure the effect of them on cell proliferation, apoptosis, and migration.
resultMicroarray analysis identified lncRNAs, miRNAs, and mRNAs differentially expressed in PTC and normal cells, and selected lncRNA HAGLROS, miR-206, and mRNA HMGA2 as study subjects. LncRNA HAGLROS and mRNA HMGA2 were highly expressed in PTC cells while miR-206 was lowly expressed in PTC cells. LncRNA HAGLROS/HMGA2 can inhibit apoptosis of PTC cells, promote proliferation and migration, and miR-206 promotes the above process. HAGLROS and HMGA2 were negatively correlated with miR-206. shHAGLROS promoted miR-206 expression, inhibited HMGA2 expression and repressed PTC tumor growth in mice.
conclusionsHAGLROS promotes the growth of PTC by competitively binding to miR-206 to promote HMGA2 expression.
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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.