期刊论文详细信息
Journal of Biomedical Science
LncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells
Hong-yan Dai1  Lian Jin1  Ping Sun1  Wei-qi Song1  Chen Guo1 
[1] Department of Obstetrics & Gynaecology, Affiliated Hospital of inner Mongolia University For The Nationalities, Huolinhe Avenue East NO. 1742, Tongliao 028000, China
关键词: Apoptosis;    Endometrial cancer;    miR-103;    PTEN;    LncRNA-GAS5;   
Others  :  1232259
DOI  :  10.1186/s12929-015-0213-4
 received in 2015-06-16, accepted in 2015-10-16,  发布年份 2015
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【 摘 要 】

Background

Growth arrest-specific 5 (GAS5) was reported to be implicated and aberrantly express in multiple cancers. However, the expression and mechanism of action of GAS5 were largely poor understood in endometrial carcinoma.

Results

According to the result of real-time reverse-transcriptase polymerase chain reaction (RT-PCR) and flow cytometry analysis, we identified that GAS5 was down-regulated in endometrial cancer cells and stimulated the apoptosis of endometrial cancer cells. To investigate the expression of GAS5, PTEN and miR-103, RT-PCR was performed. And we found that the expression of PTEN was up-regulated when endometrial cancer cells overexpressed GAS5. The prediction of bioinformatics online revealed that GAS5 could bind to miR-103, which was further found to be regulated by GAS5. Finally, we found that miR-103 mimic could decrease the mRNA and protein levels of PTEN through luciferase reporter assay and western blotting, and GAS5 plasmid may reverse this regulation effect in endometrial cancer cells.

Conclusion

In summary, we demonstrate that GAS5 acts as an tumor suppressor lncRNA in endometrial cancer. Through inhibiting the expression of miR-103, GAS5 significantly enhanced the expression of PTEN to promote cancer cell apoptosis, and, thus, could be an important mediator in the pathogenesis of endometrial cancer.

【 授权许可】

   
2015 Guo et al.

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