类泛素蛋白FAT10在胰腺癌中的表达及生物学作用

Expression and biological role of ubiquitin protein FAT10in pancreatic cancer

目的研究胰腺癌中类泛素蛋白FAT10的表达和功能作用及其分子机制。方法PATU898细胞经电穿孔法分别转染FAT10siRNA和重组表达载体pcDNA3.1-FAT10，运用CellCountingKit-8行细胞增殖活化能力检测，流式检测细胞周期和细胞凋亡，Westermblot检测PI3K/Akt信号通路的变化。结果沉默癌细胞中FAT10表达后，胰腺癌细胞增殖活性显著降低，但其对细胞周期分布无明显影响，细胞凋亡率升高，PI3K/Akt信号表达下调；促进FAT10在细胞中表达后，以上变化趋势相反。结论FAT10可通过上调PI3K/Akt信号通路表达，促进胰腺癌细胞增殖，减少细胞凋亡。

Objective To study the expression and function of ubiquitin-like protein FAT10in pancreatic cancer and its molecular mechanism.Methods Human pancreatic cancer PATU898cells were transfected into FAT10siRNA and recombinant expression vector pcDNA3.1-FAT10by electroporation,and the cell viability was detected by cell counting kit-8cell cycle.Cell cycle and apoptosis were detected by flow cytometry.The changes of PI3K/Akt signaling pathway were detected by Westerm blot.Results The proliferation of pancreatic cancer cells was significantly decreased after the expression of FAT10in cancer cells,but it had no significant effect on the cell cycle distribution.The apoptotic rate increased and the expression of PI3K/Akt signal was down-regulated.After the expression of FAT10in cells The opposite is true.Conclusion FAT10can upregulate PI3K/Akt signaling pathway to promote pancreatic cancer cell proliferation and reduce apoptosis.