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Long non-coding RNA GAS5 acts as a molecular sponge to regulate miR-23a in gastric cancer.
Minerva Medica 2016 November 10
BACKGROUND: Long non-coding RNA (lncRNAs) play critical roles in the development of cancers. LncRNA GAS5 was identified to be involved in tumorigenesis of several cancers. However, its role and function in gastric cancer (GC) remains unknown.
METHODS: The expression of GAS5, miR-23a and MT2A in 24 paired GC tissues was detected by qRT-PCR and subjected to correlation analysis. Bio-informatics analysis was performed by using DIANA Tools. Abnormal GAS5 expression was conducted in GC cells to analyze its regulation on miR-23a and MT2A via using qRT-PCR, western blot and luciferase reporter assay.
RESULTS: We showed that GAS5 expression was decreased in GC tissue and inversed correlated with up-regulated expression of miR-23a. GAS5 negatively regulated miR-23a expression in GC cells. The bio-informatics prediction showed putative miR-23a binding sites within GAS5 transcripts. Furthermore, our data indicated the positive regulation of GAS5 on the miR-23a target, MT2A, wherein GAS5 suppressed the negative regulation of miR-23a on MT2A by binding its 3'UTR. Additionally, the expression of MT2A was also decreased in GC tissues, showing a positive or negative correlation with GAS5 or miR-23a, respectively.
CONCLUSION: These observations suggested that GAS5 could act as a ceRNA play critical roles in GC pathogenesis and might serve as a potential therapeutic target for the treatment of gastric cancer.
METHODS: The expression of GAS5, miR-23a and MT2A in 24 paired GC tissues was detected by qRT-PCR and subjected to correlation analysis. Bio-informatics analysis was performed by using DIANA Tools. Abnormal GAS5 expression was conducted in GC cells to analyze its regulation on miR-23a and MT2A via using qRT-PCR, western blot and luciferase reporter assay.
RESULTS: We showed that GAS5 expression was decreased in GC tissue and inversed correlated with up-regulated expression of miR-23a. GAS5 negatively regulated miR-23a expression in GC cells. The bio-informatics prediction showed putative miR-23a binding sites within GAS5 transcripts. Furthermore, our data indicated the positive regulation of GAS5 on the miR-23a target, MT2A, wherein GAS5 suppressed the negative regulation of miR-23a on MT2A by binding its 3'UTR. Additionally, the expression of MT2A was also decreased in GC tissues, showing a positive or negative correlation with GAS5 or miR-23a, respectively.
CONCLUSION: These observations suggested that GAS5 could act as a ceRNA play critical roles in GC pathogenesis and might serve as a potential therapeutic target for the treatment of gastric cancer.
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