| Objective: Glioma is a malignant tumor of the central nervous system with complex pathogenesis,difficult operation and high postoperative recurrence rate.There is still no effective treatment method.Changes in the expression of molecular diagnostic markers and their effects on tumor biology have now been applied in the diagnosis,classification and more accurate prognosis of gliomas.It is of great significance to explore more and more effective molecular targets for the treatment of glioma.Long non-coding RNA DDX11-AS1 has been shown to promote tumor development,however,the potential regulatory role in glioma remains to be analyzed and elucidated.This study aims to explore the expression and prognosis of long non-coding RNA DDX11-AS1 in glioma,to clarify the biological function of DDX11-AS1 on glioma cells,and to explore its potential molecular mechanism.Methods: 1)The expression differences of DDX11-AS1 in gliomas were identified by bioinformatics analysis and q-PCR detection of clinical samples,and the correlation of expression levels with patient survival and other clinical characteristics was further analyzed;2)By constructing DDX11-AS1 knockdown and overexpression glioma cell model,the Transwell assay and wound healing assay were used to detect the effect of DDX11-AS1 on cell migration,MTT assay and clone formation assay were used to detect the effect on cell proliferation,and nude mice were used to observe the role of DDX11-AS1 in tumor growth in vivo;3)The CHIRP-MS technology and Star Base V2.0 prediction analysis were used to screen the potential binding RNA-binding proteins of DDX11-AS1,and RNA immunoprecipitation experiments was used to verify the binding effect;4)Western Blot was used to detect the expression changes of downstream pathway proteins.Results: 1)The expression level of DDX11-AS1 in glioma tissue was higher than that in normal control tissue samples,and the expression level gradually increased with the increase of glioma grade.The prognoses of glioma patients with high DDX11-AS1 expression were worse than that of patients with low expression.The expression level of DDX11-AS1 was closely related to the WHO grade,IDH status,1p19 q codeletion and age of glioma patients;2)DDX11-AS1 knockdown inhibited the proliferation and migration of glioma cells,promoted apoptosis,and inhibited EMT process,Wnt/β-catenin and AKT pathways.Overexpression of DDX11-AS1 promoted proliferation and migration of glioma cells,promoted tumor growth in vivo,and activated EMT process,Wnt/β-catenin and AKT pathways;3)DDX11-AS1 interacted with HNRNPC and positively regulated HNRNPC expression.HNRNPC was highly expressed in glioma,and patients with high expression had poor prognoses.HNRNPC knockdown inhibited glioma cell proliferation and migration,EMT process,Wnt/β-catenin and AKT pathways.HNRNPC knockdown attenuated the proliferation,migration and tumorigenesis effects of DDX11-AS1 overexpression,and reduced the activation of EMT process,Wnt/β-catenin and AKT pathways.Conclusions: 1)DDX11-AS1 is highly expressed in glioma tissues,and patients with high DDX11-AS1 expression have worse prognoses than those with low DDX11-AS1 expression;2)DDX11-AS1 promotes the proliferation,migration and growth of glioma cells,and activates the EMT process,Wnt/β-catenin and AKT pathways;3)The interaction between DDX11-AS1 and HNRNPC regulates the EMT process,Wnt/β-catenin and AKT pathways to affect the development of glioma. |
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