Long non-coding RNA linc00645 promotes TGF-β-induced epithelial-mesenchymal transition by regulating miR-205-3p-ZEB1 axis in glioma

被引:60
作者
Li, Chenlong [1 ]
Zheng, Hongshan [1 ]
Hou, Weiliang [1 ]
Bao, Hongbo [1 ]
Xiong, Jinsheng [1 ]
Che, Wanli [1 ]
Gu, Yifei [1 ]
Sun, Haiming [2 ,3 ]
Liang, Peng [1 ]
机构
[1] Harbin Med Univ, Canc Hosp, Dept Neurosurg, Harbin 150001, Heilongjiang, Peoples R China
[2] Harbin Med Univ, Lab Med Genet, Harbin 150001, Heilongjiang, Peoples R China
[3] Harbin Med Univ, Heilongjiang Higher Educ Inst, Key Lab Med Genet, Harbin 150001, Heilongjiang, Peoples R China
关键词
CANCER; METASTASIS; EXPRESSION; INVASION; ZEB1; MIR-205; CELLS; EMT;
D O I
10.1038/s41419-019-1948-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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)-beta-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-beta-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-beta. 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.
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页数:17
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