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miR-181c/d is dysregulated in gastric cancer(GC).We investigated the amplification and expression of miR-181c/d and its predicted target genes in GC.Amplification of miR-181c/d was quantified by genomic real-time PCR in GC and adjacent normal tissues,as well as the levels of mature miR-181c/d was performed by real-time PCR in the same tissues.The potential target genes of miR-181c/d were predicted using bioinformatics software.Expression of one potential target gene,PDCD4,was measured by semiquantitative RT-PCR,real-time PCR,and immunohistochemistry.Next,the relationship between miR181c/d expression and PDCD4 expression was analyzed.Results indicated that the amplification and expression of miR-181c/d were significantly higher in GC than in adjacent normal tissues(primary miR-181c/d,P0.001;miR-181c,P=0.0344;miR-181d,P=0.0153),and there was a strong correlation between mature miR-181c/d and primary miR-181c/d.Thirty-two target genes were predicted,including PDCD4 which is a known tumor suppressor gene.Expression of PDCD4 was significantly down-regulated in GC as compared to adjacent normal tissues and was inversely correlated with miR-181c/d expression in GC(miR-181c and PDCD4:R=-0.496,P=0.008;miR-181d and PDCD4:R=-0.454,P=0.003).Therefore,miR-181c/d may play a pivotal role in the pathogenesis of GC by downregulating PDCD4 expression.
miR-181c / d is dysregulated in gastric cancer (GC). We investigated the amplification and expression of miR-181c / d and its predicted target genes in GC.Amplification of miR-181c / d was quantified by genomic real-time PCR in GC and adjacent normal tissues, as well as the levels of mature miR-181c / d was performed by real-time PCR in the same tissues. Potential target genes of miR-181c / d were predicted using bioinformatics software. Expression of one potential target gene, PDCD4, was measured by semiquantitative RT-PCR, real-time PCR, and immunohistochemistry .Next, the relationship between miR181c / d expression and PDCD4 expression was analyzed. Results indicated that the amplification and expression of miR- 181c / d were significantly higher in GC than in adjacent normal tissues (primary miR-181c / d, P 0.001; miR- 181c, P = 0.0344; miR- 181d, P = 0.0153) / d and primary miR-181c / d.Thirty-two target genes were predicted, including PDCD4 which is a known tumo r suppressor gene. Expression of PDCD4 was significantly down-regulated in GC as compared to adjacent normal tissues and was inversely correlated with miR-181c / d expression in GC (miR- 181c and PDCD4: R = -0.496, P = 0.008; -181d and PDCD4: R = -0.454, P = 0.003). Therefore, miR-181c / d may play a pivotal role in the pathogenesis of GC by downregulating PDCD4 expression.