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目的:研究长链非编码RNA ROR(lncRNA ROR)对胰腺癌细胞增殖凋亡的影响,并探讨其机制。方法:以胰腺癌细胞BxPC-3为研究对象,RT-PCR检测ROR与notch1的RNA水平,Western blot检测notch1蛋白的变化。通过RNAhybird及萤光素酶报告实验,探索ROR对notch1的调控机制;采用CCK-8、TUNEL检测细胞增殖凋亡的变化。结果:ROR与notch1在胰腺癌组织中均高表达,两者存在正相关性。BxPC-3细胞过表达ROR后,细胞增殖活性升高,DNA损伤阳性细胞比例降低,伴随notch1的mRNA及蛋白水平升高。萤光素酶报告实验显示:ROR可与notch1的调控因子miR-137结合并抑制其活性。将ROR与si-notch1共转染BxPC-3细胞,与对照组相比,pcDNA-ROR+si-notch1组细胞增殖活性降低,TUNEL阳性细胞比例增加,差异均具有统计学意义。结论:lncRNA ROR通过促进notch1蛋白表达,调控胰腺癌细胞的增殖凋亡。
Objective: To investigate the effect of long chain non-coding RNA ROR (lncRNA ROR) on the proliferation and apoptosis of pancreatic cancer cells and to explore its mechanism. Methods: Pancreatic cancer BxPC-3 cells were used as experimental materials. The mRNA levels of ROR and notch1 were detected by RT-PCR and the changes of notch1 protein by Western blot. RNAhybird and luciferase reporter assays were used to explore the regulation mechanism of ROR on notch1. The changes of cell proliferation and apoptosis were detected by CCK-8 and TUNEL. Results: Both ROR and notch1 were highly expressed in pancreatic cancer tissues, and there was a positive correlation between them. The overexpression of ROR in BxPC-3 cells increased the cell proliferation activity, decreased the percentage of DNA damage-positive cells, and increased the mRNA and protein level of notch1. Luciferase reporter assay showed that ROR could bind to miR-137, a regulator of notch1, and inhibit its activity. Compared with the control group, the cell proliferation activity and the percentage of TUNEL positive cells in pcDNA-ROR + si-notch1 group were co-transfected with ROR and si-notch1, the difference was statistically significant. Conclusion: The lncRNA ROR regulates the proliferation and apoptosis of pancreatic cancer cells by promoting the expression of notch1 protein.