Yang Su1, Chao Liang, Qunfu Yang. 1. 2nd Department of Neurosurgery, Xingtai People's Hospital, Xingtai, Hebei Province, China.
Abstract
PURPOSE: To explore the effect of LncRNA MALAT1 on the growth of glioma cells and its related mechanism. METHODS: The expression of LncRNA MALAT1 and its target gene miR-613 in glioma cells was detected by RT-PCR, and the proliferation, invasion and apoptosis rates and the expression of related proteins were detected by CCK-8, invasion and apoptosis rate tests. RESULTS: The results of qRT-PCR showed that LncRNA MALAT1 was up-regulated and miR-613 was down-regulated in glioma tissues and cells, and LncRNA MALAT1 was negatively correlated with miR-613. Cell tests confirmed that LncRNA MALAT1 played a role in promoting oncogene, including promoting proliferation and invasion of glioma cells and promoting apoptosis. Bioinformatics prediction and subsequent experiments proved that miR-613 was the direct target of LncRNA MALAT1. Furthermore, the proliferation and invasion ability of glioma cells were evidently inhibited, the apoptosis rate was evidently enhanced, and the expressions of pro-apoptosis related proteins bax and Cle-Caspase-3 were up-regulated while the expression of anti-apoptosis related protein bcl-2 was down-regulated. CONCLUSION: LncRNA MALAT1 can promote the proliferation and invasion of glioma cells and inhibit the apoptosis of glioma cells by sponging miR-613. LncRNA MALAT1 can be applied as a new potential target for glioma treatment.
PURPOSE: To explore the effect of LncRNA MALAT1 on the growth of glioma cells and its related mechanism. METHODS: The expression of LncRNA MALAT1 and its target gene miR-613 in glioma cells was detected by RT-PCR, and the proliferation, invasion and apoptosis rates and the expression of related proteins were detected by CCK-8, invasion and apoptosis rate tests. RESULTS: The results of qRT-PCR showed that LncRNA MALAT1 was up-regulated and miR-613 was down-regulated in glioma tissues and cells, and LncRNA MALAT1 was negatively correlated with miR-613. Cell tests confirmed that LncRNA MALAT1 played a role in promoting oncogene, including promoting proliferation and invasion of glioma cells and promoting apoptosis. Bioinformatics prediction and subsequent experiments proved that miR-613 was the direct target of LncRNA MALAT1. Furthermore, the proliferation and invasion ability of glioma cells were evidently inhibited, the apoptosis rate was evidently enhanced, and the expressions of pro-apoptosis related proteins bax and Cle-Caspase-3 were up-regulated while the expression of anti-apoptosis related protein bcl-2 was down-regulated. CONCLUSION: LncRNA MALAT1 can promote the proliferation and invasion of glioma cells and inhibit the apoptosis of glioma cells by sponging miR-613. LncRNA MALAT1 can be applied as a new potential target for glioma treatment.