METTL3 inhibits LINC00312 to suppress osteoporosis progression in a YTHDF2‑dependent manner
Wang Y., Tian Y., Yao G.
Animal Study, published in Int J Mol Med (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Int J Mol Med (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41268604
- PMCID
- PMC12668781
- DOI
- 10.3892/ijmm.2025.5699
- Citations
- 1
Abstract (original English)
The regulation of methylation and non‑coding RNAs plays important roles in the pathogenesis of osteoporosis. Most microRNAs (miRNAs or miRs) exert their biological functions through target genes. Long non‑coding RNAs function as competing endogenous RNAs. hFOB 1.19 cells were transfected with miR‑4765, LINC00312 and METTL3‑related molecules. LINC00312 and miR‑4765 expression was detected by PCR, whereas cleaved caspase 3 and FOXK2/SFRP1 levels were detected by western blotting. Micro‑computed tomography was used to detect the bone microstructure. Diabetic mice received treatments targeting METTL3 and LINC00312. FOXK2/SFRP1 expression was detected using PCR and immunohistochemistry. The results showed that miR‑4765 overexpression reduced FOXK2/SFRP1 and cleaved caspase 3 expression, causing cell apoptosis. LINC00312 inhibition was observed both in vitro and in vivo . LINC00312 binds directly to miR‑4765, whereas miR‑4765 binds directly to FOXK2/SFRP1. METTL3 and YTHDF2 directly bind LINC00312 and reduce its expression by altering its methylation levels. In conclusion, LINC00312 promotes the apoptosis of hFOB 1.19 cells by targeting the miR‑4765/FOXK2/SFRP1 axis, and METTL3 regulates LINC00312 expression in a YTHDF2‑dependent manner.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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