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QKI deficiency maintains glioma stem cell stemness by activating the SHH/GLI1 signaling pathway.
Cellular Oncology ( IF 6.6 ) Pub Date : 2019-07-10 , DOI: 10.1007/s13402-019-00463-x Bo Han 1, 2, 3 , Ruijia Wang 1, 3 , Yongjie Chen 1, 3 , Xiangqi Meng 1, 3 , Pengfei Wu 1, 3 , Ziwei Li 1, 3 , Chunbin Duan 1, 3 , Qingbin Li 1, 3 , Yang Li 1, 3 , Shihong Zhao 1, 3 , Chuanlu Jiang 1, 3 , Jinquan Cai 1, 3
中文翻译:
QKI 缺乏通过激活 SHH/GLI1 信号通路维持胶质瘤干细胞干细胞。
更新日期:2019-07-10
Cellular Oncology ( IF 6.6 ) Pub Date : 2019-07-10 , DOI: 10.1007/s13402-019-00463-x Bo Han 1, 2, 3 , Ruijia Wang 1, 3 , Yongjie Chen 1, 3 , Xiangqi Meng 1, 3 , Pengfei Wu 1, 3 , Ziwei Li 1, 3 , Chunbin Duan 1, 3 , Qingbin Li 1, 3 , Yang Li 1, 3 , Shihong Zhao 1, 3 , Chuanlu Jiang 1, 3 , Jinquan Cai 1, 3
Affiliation
Purpose
Glioblastoma (GBM) stem cells (GSCs) have been found to be the main cause of malignant GBM progression. It has also been found that Quaking homolog (QKI) plays a predominant role in driving GBM development. Here, we aimed to asses the role of QKI in maintaining GSC stemness and inducing the invasiveness of GBM cells.Methods
Public databases were used to assess the expression of QKI and its correlation with stemness markers in primary GBMs. The CRISPR-Cas9 technology was used to generate QKI knockout GBM cells, and RNA immunoprecipitation was used to assess QKI-GLI1 protein-mRNA interactions. In addition, in vitro and in vivo GBM cell proliferation, migration, xenografting and neurosphere formation assays were performed.Results
Using public GBM databases, QKI was identified as a potential GSC regulator. We found that QKI could inhibit stem-like cell (SLC) stemness and prolong the survival of xenografted mice. Mechanistically, we found that QKI knockout increased the GLI Family Zinc Finger 1 (GLI1) mRNA level, which is essential for maintaining the self-renewal ability of GSCs. In addition, we found that QKI knockout activated the Hedgehog signaling pathway via Tra-2 and GLI response element (TGE)-specific GLI1 mRNA disruption.Conclusion
Our data indicate that upregulation of GLI1 induced by QKI deficiency maintains GSC stemness and enhances the invasiveness of GBM cells, thereby hinting at new options for the treatment of GBM.中文翻译:
QKI 缺乏通过激活 SHH/GLI1 信号通路维持胶质瘤干细胞干细胞。