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Effects of small nucleolar RNA SNORD44 on the proliferation, apoptosis and invasion of glioma cells.
Histochemistry and Cell Biology ( IF 2.3 ) Pub Date : 2020-02-15 , DOI: 10.1007/s00418-020-01848-y
Xian-Ru Xia 1 , Wen-Cui Li 1 , Zong-Tao Yu 1 , Jie Li 1 , Chun-Yan Peng 1 , Li Jin 1 , Guo-Lin Yuan 1
Affiliation  

To master the effect of small nucleolar RNA, SNORD44, on the proliferation, apoptosis and invasion of glioma cells and its relevant mechanism. SNORD44 and GAS5 expression in glioma tissues and cells was detected through qRT-PCR. Then, the glioma cell lines (U87 and U251) were divided into different groups with different treatments. Cell proliferation was determined by MTT assay, while the abilities of the cell migration and invasion were measured by wound-healing test and Transwell assay, respectively. Cell apoptosis were detected by flow cytometry and TUNEL assay. The expression of apoptosis proteins was quantified through Western blotting. Finally, the xenograft models were established on nude mice to investigate the effects of SNORD44 on the growth of glioma and the expressions of Ki67, MMP2 and MMP9 in vivo. SNORD44 and GAS5 were down-regulated in glioma tissues and cells in a positive correlation. Either SNORD44 or GAS5 overexpression decreased the proliferation, invasion and migration of U87 and U251 cells with the up-regulation of apoptosis rates, as well as the expressions of cleaved PARP, caspase 3, caspase 8 and caspase 9. Moreover, the in vivo experiment showed that overexpression of SNORD44 blocked the growth of glioma xenograft in nude mice accompanying with the inhibition of Ki67, MMP2 and MMP9 expressions. The combination overexpression of SNORD44 and GAS5 gained better inhibitory effects on glioma cells. Overexpression of SNORD44 and GAS5 activate the caspase-dependent apoptosis pathway to facilitate the apoptosis with the inhibited proliferation, invasion and migration of glioma cells.

中文翻译:

小核仁RNA SNORD44对神经胶质瘤细胞增殖,凋亡和侵袭的影响。

掌握小核仁RNA SNORD44对神经胶质瘤细胞增殖,凋亡和侵袭的影响及其机制。通过qRT-PCR检测神经胶质瘤组织和细胞中SNORD44和GAS5的表达。然后,将神经胶质瘤细胞系(U87和U251)分成不同的组,进行不同的处理。用MTT法测定细胞增殖,用伤口愈合试验和Transwell法测定细胞迁移和侵袭能力。流式细胞仪和TUNEL法检测细胞凋亡。通过Western印迹定量凋亡蛋白的表达。最后,在裸鼠上建立异种移植模型,以研究SNORD44对神经胶质瘤生长以及体内Ki67,MMP2和MMP9表达的影响。SNORD44和GAS5在神经胶质瘤组织和细胞中呈正相关下调。SNORD44或GAS5的过表达均会降低U87和U251细胞的增殖,侵袭和迁移,并导致细胞凋亡率的上调以及裂解的PARP,caspase 3,caspase 8和caspase 9的表达。此外,体内实验结果表明SNORD44的过表达阻止了胶质瘤异种移植物在裸鼠体内的生长,并同时抑制了Ki67,MMP2和MMP9的表达。SNORD44和GAS5的组合过表达对神经胶质瘤细胞获得更好的抑制作用。SNORD44和GAS5的过表达激活了caspase依赖的凋亡途径,从而促进了细胞凋亡,同时抑制了胶质瘤细胞的增殖,侵袭和迁移。
更新日期:2020-04-21
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