ArticleFrontiers in genetics2026
HOTAIR regulates osteogenic-adipogenic differentiation imbalance through the miR-217/DKK1-mediated Wnt/β-catenin pathway in SONFH-BMSCs.
Article in Frontiers in genetics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Steroid-induced osteonecrosis of the femoral head (SONFH) is characterized by disrupted osteogenic and adipogenic differentiation of bone marrow mesenchymal stem cells (BMSCs). The long noncoding RNA HOTAIR is aberrantly upregulated in SONFH-BMSCs, yet its functional role in the differentiation imbalance remains incompletely understood. In this study, we investigated whether HOTAIR silencing could restore the differentiation balance in SONFH-BMSCs and clarify the underlying regulatory mechanism. Methods: HOTAIR was knocked down in SONFH-BMSCs using small interfering RNA (si-HOTAIR). Osteogenic differentiation was assessed using alkaline phosphatase (ALP) and Alizarin Red S (ARS) staining, while adipogenic differentiation was evaluated using Oil Red O staining. Expression of lineage-specific markers and Wnt pathway components was measured using qRT-PCR and Western blotting. The interactions among HOTAIR, miR-217, and DKK1 were validated through dual-luciferase reporter and rescue experiments. Results: HOTAIR silencing significantly enhanced osteogenic differentiation, as evidenced by increased ALP activity, mineralization, and upregulation of RUNX2, BMP2, and Osterix, while concurrently suppressing adipogenic differentiation, with reduced lipid droplet formation and downregulation of PPARγ, C/EBPα, and Adipsin. Mechanistically, HOTAIR acted as a candidate competing endogenous RNA (ceRNA) by sponging miR-217, thereby relieving miR-217-mediated repression of DKK1 and inhibiting Wnt/β-catenin signaling. HOTAIR knockdown restored miR-217 availability, decreased DKK1 expression, and enhanced β-catenin expression. Conclusion: HOTAIR inhibition rebalances osteogenic and adipogenic differentiation of SONFH-BMSCs via the miR-217/DKK1/Wnt/β-catenin axis. These findings identify HOTAIR as an important molecular regulator of BMSC fate determination and provide mechanistic insights into ceRNA-mediated regulation in SONFH pathogenesis.
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.