國家衛生研究院 NHRI:Item 3990099045/9129

NHRI > Institute of Biomedical Engineering and Nanomedicine > Chung-Shi Yang > Periodical Articles > Item 3990099045/9129

Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/9129

Title:	Depletion of B cell CLL/Lymphoma 11B gene expression represses glioma cell growth
Authors:	Liao, CK;Fang, KM;Chai, K;Wu, CH;Ho, CH;Yang, CS;Tzeng, SF
Contributors:	Institute of Biomedical Engineering and Nanomedicine
Abstract:	B cell CLL/lymphoma 11B (Bcl11b), a C2H2 zinc finger transcription factor, not only serves as a critical regulator in development but also plays the controversial role in T cell acute lymphoblastic leukemia (T-ALL). We previously found that the enriched expression of Bcl11b was detected in high tumorigenic C6 glioma cells. However, the role of Bcl11b in glioma malignancy and its mechanisms remains to be uncovered. In this study, using the lentivirus-mediated knockdown (KD) approach, we found that Bcl11b KD in tumorigenic C6 cells reduced the cell proliferation, colony formation, and migratory ability. The results were further verified using two human malignant glioma cell lines, U87 and U251 cells. A cyclin-dependent kinase inhibitor p21, a known Bcl11b target, was significantly upregulated in tumorigenic C6, U87, and U251 cells after Bcl11b KD. Cellular senescence was observed by examination of the β-galactosidase activity in U87 and U251 cells with Bcl11b KD. Reduced expression of stemness gene Sox-2 and its downstream effector Bmi-1 was also observed in U87 and U251 cells with Bcl11b KD. These results suggest that the ablation of Bcl11b gene expression induced glioma cell senescence. Propidium iodide (PI) staining combined with flow cytometry analysis also showed that Bcl11b KD led to the cell cycle arrest of U87 and U251 cells at the G0/G1 or at the S phase, indicating that Bcl11b is required for glioma cell cycle progression. Together, this is the first study to show that the inhibition of Bcl11b suppresses glioma cell growth by regulating the expression of the cell cycle regulator p21 and stemness-associated genes (Sox-2/Bmi-1).
Date:	2016-08
Relation:	Molecular Neurobiology. 2016 Aug;53(6):3528-3539.
Link to:	http://dx.doi.org/10.1007/s12035-015-9231-1
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0893-7648&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000379707600002
Cited Times(Scopus):	http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84931843723
Appears in Collections:	[Chung-Shi Yang] Periodical Articles

Files in This Item:

File	Description	Size	Format
SCP84931843723.pdf		7788Kb	Adobe PDF	518	View/Open

Loading...