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

Chen Guo,Ping Sun,Wei-Qi Song,Lian Jin,Hong-Yan Dai

doi:10.1186/s12929-015-0213-4

Chen Guo, Ping Sun + Show 3 more

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https://doi.org/10.1186/s12929-015-0213-4

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Abstract

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.

Highlights

Growth arrest-specific 5 (GAS5) was reported to be implicated and aberrantly express in multiple cancers
LncRNA-GAS5 was down-regulated in endometrial cancer cells and induced apoptosis of endometrial cancer cells To explore the role of long non-coding RNAs (lncRNAs)-GAS5 in endometrial cancer cells, we examined the relative expression of lncRNA-GAS5 in tissues from endometrial cancer patients and health controls with qRT-PCR
As lncRNA-GAS5 was reported to involve in apoptosis of several cancers, we detected the effect of lncRNA-GAS5 overexpression on apoptosis of endometrial cancer cell lines HHUA and JEC

Summary

Introduction

Growth arrest-specific 5 (GAS5) was reported to be implicated and aberrantly express in multiple cancers. The expression and mechanism of action of GAS5 were largely poor understood in endometrial carcinoma. Endometrial carcinoma, one of the most frequent gynecologic malignancy, is the fourth most common cancer of women in the United States [26]. The molecular mechanisms of endometrial carcinogenesis have been poorly understood. Mounting evidence indicated that the aberrant expression of some lncRNAs might play an important functional role in cancer biology [8]. LncRNAs can act as proto-oncogenes (e.g., HOTAIR) or tumor suppressor genes (e.g., GAS5 (growth arrest-specific transcript 5)) in tumorigenesis [11, 20]. GAS5 was identified using a functional screen through its ability to suppress apoptosis in a

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