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Downregulation of miR-199a-3p in Hepatocellular Carcinoma and Its Relevant Molecular Mechanism via GEO, TCGA Database and In Silico Analyses

机译:通过Geo,TCGA数据库和硅分析中肝细胞癌MiR-199A-3P的下调及其相关分子机制

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摘要

Existing reports have demonstrated that miR-199a-3p plays a role as a tumor suppressor in a variety of human cancers. This study aims to further validate the expression of miR-199a-3p in HCC and to explore its underlying mechanisms by using multiple data sets. Chip data or sequencing data and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were integrated to assess the expression of miR-199a-3p in HCC. The potential targets and transcription factor regulatory network of miR-199a-3p in HCC were determined and possible biological mechanism of miR-199a-3p was analyzed with bioinformatics methods. In the results, miR-199a-3p expression was significantly lower in HCC tissues compared to normal tissues according to chip data or sequencing data and qRT-PCR. Moreover, 455 targets of miR-199a-3p were confirmed, and these genes were involved in the PI3K-Akt signaling pathway, pathways in cancer, and focal adhesions. LAMA4 was considered a key target of miR-199a-3p. In CMTCN, 11 co-regulatory pairs, 3 TF-FFLs, and 2 composite-FFLs were constructed. In conclusion, miR-199a-3p was down regulated in HCC and LAMA4 may be a potential target of miR-199a-3p in HCC.
机译:现有的报告表明,MiR-199A-3P在各种人类癌症中发挥作用作为肿瘤抑制作用。本研究旨在通过使用多个数据集进一步验证MIR-199A-3P的表达,并探索其潜在机制。芯片数据或测序数据和定量逆转录聚合酶链反应(QRT-PCR)被整合以评估HCC中miR-199A-3P的表达。确定了MIR-199A-3P的潜在靶标和转录因子调节网络,并用生物信息化方法分析了MIR-199A-3P的可能生物机制。结果,与根据芯片数据或测序数据和QRT-PCR的正常组织相比,MiR-199A-3P表达在HCC组织中显着降低。此外,确认了MiR-199A-3P的455个靶标,这些基因参与了PI3K-AKT信号通路,癌症途径和局灶性粘连。喇嘛4被认为是MiR-199A-3P的关键目标。在CMTCN中,构建了11个共调节对,3个TF-FFL和2个复合FFL。总之,MIR-199A-3P在HCC中调节,喇嘛可能是HCC中MIR-199A-3P的潜在目标。

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