TRIB3 confers glioma cell stemness via interacting with ?-catenin.
Here, we aim to explore whether tribbles pseudokinase 3 (TRIB3) enhances glioma cell stemness. TRIB3 was overexpressed in glioma tissues and cell-formed spheres, positively correlated with the size and grade. Additionally, TRIB3 expression displayed a negative correlation with the overall survival rate of glioma patients. Moreover, TRIB3 knockdown reduced the ... stemness of nonadherent spheres, evident by the decreased sphere-forming ability, stemness master expression, and ALDH1 activity, while TRIB3 overexpression enhanced the stemness of adherent cells, which was rescued by ?-catenin knockdown. Mechanistically, TRIB3 activated ?-catenin signaling via physically interacting with ?-catenin. This study suggests that the TRIB3-?-catenin interaction is responsible for glioma cell stemness.
Mesh Terms:
Adult, Cell Cycle Proteins, Cell Line, Tumor, Female, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Glioma, Humans, Male, Middle Aged, Neoplastic Stem Cells, Protein Serine-Threonine Kinases, Repressor Proteins, Wnt Signaling Pathway, beta Catenin
Adult, Cell Cycle Proteins, Cell Line, Tumor, Female, Gene Expression Regulation, Neoplastic, Gene Knockdown Techniques, Glioma, Humans, Male, Middle Aged, Neoplastic Stem Cells, Protein Serine-Threonine Kinases, Repressor Proteins, Wnt Signaling Pathway, beta Catenin
Environ Toxicol
Date: Jun. 01, 2020
PubMed ID: 31995275
View in: Pubmed Google Scholar
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