ArticleJournal of orthopaedic surgery and research2025
Transcriptome sequencing-based analysis of the molecular mechanism underlying the effect of lncRNA AC003090.1 on osteoporosis.
Article in Journal of orthopaedic surgery and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
objectiveTo analyze changes in the expression of osteoporosis (OP)-related genes across different bone types based on transcriptome sequencing, and to identify the key molecules and mechanisms involved in the progression of OP in order to better understand this process.
methodsTen pairs of postmenopausal patients with osteoporosis (OP) and non-osteoporotic (non-OP) volunteers were included. Transcriptome sequencing was performed on six pairs of spongy and cortical bone tissues. The expression of FOXP1 was detected using quantitative real-time PCR (RT-qPCR) and receiver operating characteristic (ROC) curves. Magnetic-activated cell sorting was conducted, and the expression levels of AC003090.1, miR-203a-3p, and FOXP1 were measured using RT-qPCR. Human bone marrow stem cells (hBMSCs) were infected with a lentivirus carrying the AC003090.1 expression plasmid. The expression levels of Runx2, Opn, and Ocn in spongy and cortical bone samples, as well as in post-infection cells, were assessed through RT-qPCR. The expression levels of GSK-3β, β-catenin, and c-Myc were evaluated by performing RT-qPCR and Western blot analysis.
resultA total of 2,102 out of 2,827 differentially expressed genes (DEGs) were identified between the cortical bone samples from patients with osteoporosis (OP) and the cortical/spongy bone samples of the control group. Among these, 1,482 were significantly up-regulated, and 620 were significantly down-regulated, while 1,146 were significantly up-regulated and 1,681 were significantly down-regulated. The expression of FOXP1 in tissue and bone tissue-derived mesenchymal stem cells (MSCs) from patients with OP was significantly lower than that in patients without OP. FOXP1 levels in bone tissue (cortical bone AUC = 0.825, P = 0.01405; spongy bone AUC = 0.800, P = 0.02338) could serve as predictors of OP. In addition, the overexpression of AC003090.1 significantly enhanced the transcription levels of Runx2, Opn, and Ocn; significantly upregulated the expression levels of β-catenin and c-Myc; and inhibited the expression of GSK-3β. Transfection with miR-203a-3p mimics and FOXP1 small interfering RNA reversed the effect of AC003090.1 on GSK-3β/β-catenin/c-Myc signaling.
conclusionFOXP1, as a molecular mediator of AC003090.1, affects the GSK-3β/β-catenin/c-Myc signaling pathway and promotes the osteogenic differentiation of hBMSCs, thus playing a key role in the progression of OP.
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.