LncRNA MIR22HG negatively regulates miR-141-3p to enhance DAPK1 expression and inhibits endometrial carcinoma cells proliferation - 11/06/18
, Xin An b, Jingxia Li a, Qiaozhen Liu c, Wenli Liu aBienvenue sur EM-consulte, la référence des professionnels de santé.
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Highlights |
• | MIR22HG act as a tumor suppressor in EC. |
• | MIR22HG directly interacted with miR-141-3p in EC. |
• | MIR22HG/miR-141-3p/DAPK1 axis play important roles in EC tumorigenesis. |
Abstract |
Emerging evidence has indicated that long non-coding RNAs (lncRNAs) play critical roles in tumor development and progression. Recent studies reported that lncRNA MIR22HG could play important roles in hepatocellular carcinoma and lung cancer progression. However, the expression and underlying mechanism of MIR22HG in endometrial cancer (EC) remain unclear. In the present study, qRT-PCR showed that MIR22HG expression was significantly downregulated in EC tissues. In vitro function assays showed that increased MIR22HG expression significantly inhibited EC cells proliferation, induced EC cells apoptosis, and arrested EC cells in G0/G1 phase. Furthermore, miR-141-3p was identified and confirmed to be the target of MIR22HG. Subsequently, DAPK1 was confirmed to be regulated by MIR22HG and miR-141-3p, and could play a positive role in inhibiting EC cells proliferation. Collectively, these data demonstrated that lncRNA MIR22HG could act as a tumor suppressor and inhibited EC cells proliferation through regulating miR-141-3p/DAPK1 axis, which provides a new therapeutic target for EC treatment.
Le texte complet de cet article est disponible en PDF.Keywords : LncRNA MIR22HG, miR-141-3p, DAPK1, Endometrial carcinoma
Plan
Vol 104
P. 223-228 - août 2018 Retour au numéro
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