ArticleExperimental and therapeutic medicine2015
Signal transducer and activator of transcription 3 regulates CCAAT-enhancer-binding homologous protein expression in osteoblasts through upregulation of microRNA-205.
Article in Experimental and therapeutic medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- JI017 induces cell line specific anticancer effects in hepatocellular carcinoma by suppressing the STAT3 signaling pathway.Molecular biology reports · 2025Article
- Insights into the underlying pathogenesis and therapeutic potential of endoplasmic reticulum stress in degenerative musculoskeletal diseases.Military Medical Research · 2023Review
- Systematic analysis of lncRNAs, miRNAs and mRNAs for the identification of biomarkers for osteoporosis in the mandible of ovariectomized mice.International journal of molecular medicine · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
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Abstract
The transcription factor, CCAAT-enhancer-binding protein homologous protein (CHOP), is induced by endoplasmic reticulum-stress and mediates programmed cell death. In osteoblasts, CHOP overexpression increases the rate of apoptosis, leading to osteoblastic dysfunction. However, the regulatory mechanisms underlying CHOP expression remain unclear. In the present study, western blot analysis was used to demonstrate that the activation of signal transducer and activator of transcription 3 (STAT3) inhibited the levels of the CHOP protein, whereas small interfering RNA-mediated the knockdown of STAT3 upregulated CHOP expression. Furthermore, STAT3 was shown to increase the expression level of microRNA (miR)-205. A luciferase reporter assay revealed that miR-205 was able to directly target the 3'-untranslated region of the CHOP gene to inhibit its protein expression. The miR-205 antisense largely abolished the inhibitory effect of STAT3 activation on the levels of CHOP protein. Therefore, the results demonstrated a previously unknown STAT3/miR-205/CHOP signaling pathway in osteoblasts, which may aid the understanding of the pathogenic mechanisms of associated diseases, including osteoporosis.
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