ReviewCell & bioscience2019
LncRNA MALAT1 promotes osteoarthritis by modulating miR-150-5p/AKT3 axis.
Review in Cell & bioscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
108 citing papers in PubMed, 1 synthesis or guideline pooled it, 174 citations in OpenAlex.
- Allelic expression imbalance in articular cartilage and subchondral bone refined genome-wide association signals in osteoarthritis.Rheumatology (Oxford, England) · 2023Pooled it
- lncRNA MALAT1-mediated regulation of cholesterol-oxidative stress-iron metabolic dysregulation by paeoniflorin in osteoarthritic chondrocytes.Pharmaceutical biology · 2026Article
- DNA methylation-mediated silencing of MALAT1 promotes dexamethasone-induced growth plate chondrocyte ferroptosis via miR-124-3p/LPCAT3.Journal of bioenergetics and biomembranes · 2026Article
- LINC00312 affects the progression of osteoarthritis by targeting miR-331-3p/DUSP5 axis.Journal of orthopaedic surgery and research · 2026Article
- SATB1 Exhibits a Protective Role in HAmylin-Oligomer-Induced Neuronal Damage and Cognition Decline.CNS neuroscience & therapeutics · 2026Article
- Non-coding RNAs in congenital heart disease and placental development: Bridging molecular mechanisms to clinical biomarkers and therapies.Non-coding RNA research · 2026Review
- Clinical significance of LncRNA NORAD and its potential mechanism in chronic obstructive pulmonary disease.BMC pulmonary medicine · 2026Article
- Programmed cell death in osteoarthritis.Apoptosis : an international journal on programmed cell death · 2026Review
- Identification of miRNAs Expression Characteristics and Biomarkers in Serum-Derived Exosomes of Wilson's Disease Patients.Mediators of inflammation · 2026Article
- Genome-wide gene expression analysis suggests an important regulatory role of lncRNAs in primary Sjögren's syndrome.Frontiers in immunology · 2026Article
- Role of long non-coding RNAs in cartilage development and osteoarthritis pathogenesis.European journal of medical research · 2025Review
- lncRNA PVT1 regulates chondrocyte proliferation and apoptosis through the glycolysis process mediated by miR-552-3p/PKM2 to promote osteoarthritis.In vitro cellular & developmental biology. Animal · 2025Article
- DNA hypomethylated modified lncRNA MALAT1 promotes atherosclerotic cardiovascular disease progression through NF-κB signaling pathway regulating cholesterol metabolism and inflammatory response.Biochemistry and biophysics reports · 2025Article
- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- LncRNA AC005165.1 Alleviates IL-1β-Induced Osteoarthritis via miR-199a-3p/TXNIP Axis.Biochemical genetics · 2025Article
- The Role of miR-150-5p/SOCS1 Pathway in Arsenic-Induced Pyroptosis of LX-2 Cells.Biological trace element research · 2025Article
- MiR-301b-3p targets and regulates EBF3 to impact the stem-like phenotype of breast cancer cells through glycolysis.Journal of clinical biochemistry and nutrition · 2025Article
- Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Extended abstinence from morphine alters sperm smRNA expression and prevents transmission of intergenerational phenotypes.Environmental epigenetics · 2025Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMany studies have reported that long noncoding RNAs (lncRNAs) could act as sponges for microRNAs (miRNAs) and play important roles in the regulation of osteoarthritis (OA). Yet, the underlying mechanisms of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in OA are still unclear. Therefore, we aimed to explore the regulation mechanisms of MALAT1 in OA procession.
methodsIL-1β treatment in chondrocyte was used to mimic OA in vitro. MALAT1, miR-150-5p and AKT3 expression levels were detected via qRT-PCR. The protein levels of AKT3, MMP-13, ADAMTS-5, Bax, Bcl-2, cleaved-PARP, collagen II and aggracan were measured by western blot. MTT assay was performed to detect cell proliferation ability. The apoptosis of chondrocytes was determined using flow cytometry and western blot. Luciferase assay and RNA immunoprecipitation (RIP) assays were used to confirm the relationship among MALAT1, miR-150-5p and AKT3.
resultsIn our study, MALAT1 and AKT3 were upregulated while miR-150-5p was downregulated in OA in vitro and vivo. The level of miR-150-5p was negatively correlated with that of MALAT1 or AKT3. More importantly, overexpression of MALAT1 promoted the expression of AKT3 by negatively regulating miR-150-5p. MALAT1 knockdown inhibited cell proliferation, promoted apoptosis, increased MMP-13, ADAMTS-5 expression and decreased collagen II, aggracan expression in IL-1β treated chondrocytes. MALAT1 upregulation or AKT3 overexpression enhanced proliferation, inhibited apoptosis and extracellular matrix (ECM) degradation, which was undermined by overexpression of miR-150-5p. By contrast, miR-150-5p depletion rescued the effect of MALAT1 downregulation or loss of AKT3 on IL-1β-stimulated chondrocytes.
conclusionMALAT1 was responsible for cell proliferation, apoptosis, and ECM degradation via miR-150-5p/AKT3 axis.
Indexed as
Identifiers
What OpenQuestion holds
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.