LncRNA-GAS5 induces PTEN expression through inhibiting miR-103 in endometrial cancer cells

Journal of Biomedical Science

Research

Chen Guo¹  Ping Sun¹  Hong-yan Dai¹  Wei-qi Song¹  Lian Jin¹ 

[1] Department of Obstetrics & Gynaecology, Affiliated Hospital of inner Mongolia University For The Nationalities, Huolinhe Avenue East NO. 1742, 028000, Tongliao, China;

关键词: LncRNA-GAS5;    PTEN;    miR-103;    Endometrial cancer;    Apoptosis;   

DOI  :  10.1186/s12929-015-0213-4

 received in 2015-06-16, accepted in 2015-10-16,  发布年份 2015

来源: Springer

【 摘 要 】

BackgroundGrowth 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.ResultsAccording 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.ConclusionIn 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】

CC BY   
© Guo et al. 2015