ArticleExperimental and therapeutic medicine2021
lncRNA WT1-AS is upregulated in osteoporosis and regulates the apoptosis of osteoblasts by interacting with p53.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 5 citations in OpenAlex.
- LOC100912399 regulates osteogenic differentiation of bone marrow mesenchymal stem cells through modulating p38MAPK signaling-mediated oxidative stress and apoptosis.Scientific reports · 2026Article
- Dual disease co-expression analysis reveals potential roles of estrogen-related genes in postmenopausal osteoporosis and Parkinson's disease.Frontiers in genetics · 2024Article
- Network regulatory mechanism of ncRNA on the Wnt signaling pathway in osteoporosis.Cell division · 2023Review
- Article
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5 authors at 2 institutions in 1 country.
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Abstract
In cervical cancer, cellular tumor antigen p53 (p53) interacts with long non-coding WT1 antisense RNA (WT1-AS) and this protein serves an important role in osteoporosis. The present study aimed to investigate the role of WT1-AS in osteoporosis. WT1-AS was upregulated in the plasma of patients with osteoporosis and was positively correlated with p53 expression. Altered expression of WT1-AS and p53 separated patients with osteoporosis from healthy controls. Expression levels of WT1-AS and p53 decreased with prolonged treatment. In osteoblasts, WT1-AS overexpression resulted in increased p53 expression, while WT1-AS small interfering RNA (siRNA) silencing resulted in decreased p53 expression. In addition, WT1-AS overexpression resulted in increased apoptosis rate, while WT1-AS siRNA silencing resulted in decreased apoptosis rate in osteoblasts. p53 overexpression attenuated the effects of WT1-AS siRNA silencing on cell apoptosis. Therefore, WT1-AS was upregulated during osteoporosis and regulated the apoptosis of osteoblasts by interacting with p53.
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