ArticleThe Journal of international medical research2018
Adiponectin receptor 1-mediated micro RNA-323-3p regulates functions of the MIN6 cell line via the AMP-activated protein kinase/sirtuin-1 pathway.
Article in The Journal of international medical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Effects of Cilostazol on Angiogenesis in Diabetes through Adiponectin/Adiponectin Receptors/Sirtuin1 Signaling Pathway.International journal of molecular sciences · 2022Article
- MiR-323-3p Targeting Transmembrane Protein with EGF-Like and 2 Follistatin Domain (TMEFF2) Inhibits Human Lung Cancer A549 Cell Apoptosis by Regulation of AKT and ERK Signaling Pathways.Medical science monitor : international medical journal of experimental and clinical research · 2020Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background The development of an effective treatment for type 2 diabetes mellitus is urgently needed. This study aimed to investigate the role of micro RNA (miR)-323-3p in regulating the expression of adiponectin receptor 1 (AdipoR1), as well as the insulin secretion and cell function of pancreatic MIN6 β-cells. Methods MIN6 cells were treated with miR-323-3p mimics or inhibitors, and the effects on cell growth, proliferation, mitosis, and insulin secretion were studied. The expression levels of sirtuin-1 (SIRT-1) and AMP-activated protein kinase (AMPK) genes were also assessed. Results miR-323-3p directly targeted AdipoR1, and suppressed its expression at mRNA and protein levels. It also regulated the protein expression of SIRT-1 and AMPK, which are downstream target genes of the AdipoR1 signaling pathway. miR-323-3p suppressed cell growth, proliferation, mitosis, and insulin secretion of MIN6 cells. Conclusions miR-323-3p appears to be a crucial diabetes factor that mediates its functions by inhibiting the AdipoR1/AMPK/SIRT-1 signaling pathway. Our findings suggest that targeting AdipoR1 with inhibitors of miR-323-3p is a potential approach to improve the function of islet cells.
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