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Abstract

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.

Details

Title
Effects of small nucleolar RNA SNORD44 on the proliferation, apoptosis and invasion of glioma cells
Author
Xian-Ru, Xia 1 ; Wen-Cui, Li 1 ; Zong-Tao, Yu 1 ; Li, Jie 1 ; Chun-Yan, Peng 1 ; Li, Jin 1 ; Guo-Lin, Yuan 1   VIAFID ORCID Logo 

 Taihe Hospital, Hubei University of Medicine, Department of Clinical Laboratory, Shiyan, China 
Pages
257-269
Publication year
2020
Publication date
Apr 2020
Publisher
Springer Nature B.V.
ISSN
09486143
e-ISSN
1432119X
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2390059419
Copyright
© Springer-Verlag GmbH Germany, part of Springer Nature 2020.