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Long non-coding RNA SUMO1P3 may promote cell proliferation migration and invasion of pancreatic cancer via EMT signaling pathway

机译:长的非编码RNA SUMO1P3可能通过EMT信号传导途径促进胰腺癌的细胞增殖迁移和侵袭

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摘要

Long non-coding RNAs (lncRNAs) have been suggested to serve important roles in the development of a number of human cancer types. An increasing amount of data has indicated that the lncRNA small ubiquitin-like modifier 1 (SUMO1) pseudogene 3 (SUMO1P3) has been involved in various types of human cancer. However, the function SUMO1P3 in the development of pancreatic cancer remains unclear. Firstly, reverse transcription-quantitative polymerase chain reaction was performed to determine the expression of SUMO1P3 in pancreatic cancer tissues and cell lines. Then, cell counting kit-8, wound-healing and transwell assays were conducted to explore the effect of SUMO1P3 on pancreatic cancer cell proliferation, migration and invasion. Finally, the EMT-associated proteins were evaluated by western blotting. The results of the present study revealed that SUMO1P3 expression was elevated in pancreatic tissues compared with the corresponding adjacent normal tissues. Additionally, the data indicated that the increased expression of SUMO1P3 is significantly associated with tumor progression and the poor survival of patients with pancreatic cancer. Furthermore, the present study identified that SUMO1P3 knockdown may suppress the proliferation, migration and invasion of pancreatic cancer cells. Additionally, downregulation of SUMO1P3 suppressed the epithelial-mesenchymal transition (EMT) and increased the expression of epithelial cadherin, and decreased the expression of neuronal cadherin, vimentin and β-catenin. Taken together, the results of the present study demonstrated that SUMO1P3 may participate in EMT and pancreatic cancer progression, thus suggesting that it may be a novel diagnostic and therapeutic biological target for pancreatic cancer.
机译:已经提出,长的非编码RNA(lncRNA)在许多人类癌症类型的发展中起重要作用。越来越多的数据表明,lncRNA小泛素样修饰物1(SUMO1)假基因3(SUMO1P3)已参与各种类型的人类癌症。然而,SUMO1P3在胰腺癌发展中的功能仍不清楚。首先,进行逆转录-定量聚合酶链反应,以确定SUMO1P3在胰腺癌组织和细胞系中的表达。然后,进行细胞计数试剂盒8,伤口愈合和transwell分析,以探讨SUMO1P3对胰腺癌细胞增殖,迁移和侵袭的影响。最后,通过蛋白质印迹法评估EMT相关蛋白。本研究的结果表明,与相应的邻近正常组织相比,胰腺组织中的SUMO1P3表达升高。另外,数据表明SUMO1P3表达的增加与胰腺癌患者的肿瘤进展和不良的存活率显着相关。此外,本研究发现SUMO1P3敲低可能抑制胰腺癌细胞的增殖,迁移和侵袭。此外,SUMO1P3的下调抑制了上皮-间充质转化(EMT),增加了上皮钙粘蛋白的表达,并降低了神经元钙粘蛋白,波形蛋白和β-连环蛋白的表达。两者合计,本研究的结果表明SUMO1P3可能参与EMT和胰腺癌的进展,从而表明它可能是胰腺癌的新型诊断和治疗生物学靶标。

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