LncRNA-ATB Activates P38/MAPK Pathway To Promote TGF-?1-induced Glioma Cell Invasion

Objective To explore roles of the long non-coding RNA activated by TGF-?(lnc RNA-ATB)overexpression in TGF-?1-induced glioma cell invasion and to further investigate related molecular mechanisms in glioma cells.Methods Quantitative real-time polymerase chain reaction(q RT-PCR)was used to detect the m RNA expression of related genes.Transwell assay was performed to assess the impact of lnc RNA-ATB on TGF-?1-induced glioma cells migration and invasion.Western-blot was used for detecting the protein expression of related genes.Results Compared with control,TGF-?1 apparently induced lnc RNA-ATB expression after treating glioma cells with TGF-?1 2.5 ng/ml for 24 h.Besides,TGF-?1 up-regulated lnc RNA-ATB expression in glioma cell lines LN18 and U251 was in a dose-dependent and time-dependent manner.Lnc RNA-ATB overexpression promoted glioma cells migration and invasion mediated by TGF-?1.Mechanism research found that lnc RNA-ATB promoted TGF-?1-induced glioma cells invasion through p38/MAPK pathway.p38/MAPK specific inhibitor SB203580 partly reversed lnc RNA-ATB induced glioma cells invasion mediated by TGF-?1.Conclusion TGF-?1 induced lnc RNA-ATB expression in glioma cells,and overexpression of lnc RNA-ATB promoted TGF-?1-mediated glioma cells invasion through p38/MAPK pathway.