Abstract
Accumulating evidence indicates long noncoding RNAs (lncRNA) play a vital role in tumor progression. However, the role of linc00645-induced accelerated malignant behavior in glioblastoma (GBM) remains unknown. In the present study, linc00645 expression was significantly upregulated in GBM tissues and cell lines. High level of linc00645 was associated with poor overall survival in GBM patients. Knockdown of linc00645 suppressed the proliferation, stemness, migration, invasion, and reversed transforming growth factor (TGF)-β-induced motility of glioma cell lines. Furthermore, linc00645 directly interacted with miR-205-3p and upregulated of miR-205-3p impeded efficiently the increase of ZEB1 induced by linc00645 overexpression. Moreover, knockdown of linc00645 significantly suppressed the progression of glioma cells in vivo. miR-205-3p was a target of linc00645 and linc00645 modulates TGF-β-induced glioma cell migration and invasion via miR-205-3p. Taken together, our findings identified the linc00645/miR-205-3p/ZEB1 signaling axis as a key player in EMT of glioma cells triggered by TGF-β. These data elucidated that linc00645 plays an oncogenic role in glioma and it may serve as a prognostic biomarker and a potential therapeutic target for the treatment of glioma in humans.
Highlights
Over the past few decades, glioma has been the leading cause of central nervous system malignant tumor-related deaths in China and worldwide[1]
These results indicated a significant increase of linc00645 level compared with normal brain tissues, and a positively correlation with the pathological grade of glioma in CGGA, and Gene Expression Omnibus (GEO) databse. (Fig. 1a, c and Additional file 1: Fig. S1a)
Correlation between linc00645 and miR-205-3p Using miRDB and LncBase V2. database blast prediction combined with the data from the Cancer Genome Atlas (TCGA), we found that linc00645 has several putative miRNA targets. miR-205-3p had the highest score, and accumulating evidence indicates that miR-205-3p participates in Epithelial-to-mesenchymal transition (EMT) regulation by targeting ZEB135,36
Summary
Over the past few decades, glioma has been the leading cause of central nervous system malignant tumor-related deaths in China and worldwide[1]. The growing incidence and high fatality of glioma made it urgent to elucidate the pathological mechanisms underlying its progression. It is well-known that the process underlying the occurrence of glioma is complicated, involving a lot of Epithelial-to-mesenchymal transition (EMT) is a wellrecognized integral component of invasion and migration processes[4], which is characterized by loss of cell adhesion, changing in the composition of the cytoskeleton and acquisition of migration ability and invasive traits[5,6,7]. Official journal of the Cell Death Differentiation Association
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