ArticleBioengineered2022
MicroRNA-122-3p plays as the target of long non-coding RNA LINC00665 in repressing the progress of arthritis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Integrated stress response in Behçet disease: expression analyses in peripheral blood and synovial monocytes.Rheumatology international · 2025Article
- The Role of Long Non-Coding RNA in Rheumatoid Arthritis.International journal of molecular sciences · 2025Review
- Overexpression of lncRNA LINC00665 inhibits the proliferation and chondroblast differentiation of bone marrow mesenchymal stem cells by targeting miR-214-3p.Journal of orthopaedic surgery and research · 2024Article
- Long noncoding RNA/circular RNA regulates competitive endogenous RNA networks in rheumatoid arthritis: molecular mechanisms and traditional Chinese medicine therapeutic significances.Annals of medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNAs (miRNAs) play important roles in many diseases, including rheumatoid arthritis (RA). However, the mechanisms underlying the effects of miR-122-3p-3p on RA are not distinct and require further investigation. Patients with RA and healthy controls were recruited to analyze the miR-122-3p levels. The MH7A cells were stimulated with interleukin (IL)-1β to mimic the local inflammation of RA. Cell Counting Kit-8 (CCK-8) and flow cytometry were performed to measure the viability and apoptosis of MH7A cells. Diana tools and TargetScan were used to predict the target relationships. Luciferase reporter assay was used to validate the target relationship. miR-122-3p is downregulated in RA patients and IL-1β-stimulated MH7A cells. miR-122-3p suppresses MH7A cell viability and promotes MH7A cell apoptosis. miR-122-3p targets LINC00665. LINC00665 eliminates the inhibitory effect of miR-122-3p on IL-1β-stimulated MH7A cells. Eukaryotic translation initiation factor 2 alpha kinase 1 (EIF2AK1) targets miR-122-3p. In addition, EIF2AK1 is highly expressed in patients with RA. In addition, EIF2AK1 activates the mTOR signaling pathway. miR-122-3p represses RA progression by reducing cell viability and increasing synoviocyte apoptosis.
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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 Socratic graph.