Effects of Ubiquitination on the Expression of BCL6 Protein，Cell Proliferation and Apoptosis in K562/G01 Cells.
10.19746/j.cnki.issn.1009-2137.2019.02.011
- Author:
Hui-Min TANG
1
;
Wei DING
2
;
Yi-Han DING
1
;
Jing-Jing WU
1
;
Yu-Feng LI
3
Author Information
1. Department of Hematology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian 223300, Jiangsu Province, China.
2. Department of Respiratory diseases, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian 223300, Jiangsu Province, China.
3. Department of Hematology, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian 223300, Jiangsu Province, China,E-mail:liyufen999@netease.com.
- Publication Type:Journal Article
- MeSH:
Apoptosis;
Cell Proliferation;
Humans;
Imatinib Mesylate;
K562 Cells;
Proto-Oncogene Proteins c-bcl-6;
metabolism;
Ubiquitination
- From:
Journal of Experimental Hematology
2019;27(2):379-384
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the the effects of ubiquitin-proteasome system (UPS) on BCL6 protein level，proliferation and apoptosis of cell imatinib（IM）-resistant K562/G01 cells.
METHODS:Western blot was used to detect the expression of BCL6 in K562/G01 cells before and after treatment with protease inhibitor MG-132.The RT-PCR and Western blot respectively were used to detect the mRNA and protein expression levels of BCL6 and USP2 in K562/G01 cells treated with or without ML364 (a ubiquitin-specific protease USP2 inhibitor). The effects of IM alone or in combination with ML364 on proliferation and apoptosis of K562/G01 were analysed by CCK-8 method and flow cytometry.
RESULTS:After treatment with protease inhibitor MG132, the BCL6 protein level of K562/G01 significantly increased (P<0.05). The mRNA and protein expression level of ubiquitin-specific protease USP2 in K562/G01 cell line was higher than that in K562 cell line (P<0.05). After treatment of K562/G01 with USP2 protease inhibitor ML364, the expression levels of USP2 and BCL6 proteins were down-regulated simultaneously (P<0.05) . After combination of ML364 and IM, both the proliferation inhibitory rate and the apoptosis rate of K562/G01 cells significantly increased(P<0.05).
CONCLUSION:ML364 decreases the BCL6 protein stability in K562/G01 by inhibiting the USP2-mediated deubiquitination, and down-regulate the BCL6 protein experssion, thereby increases the sensitivity of drug-resistant cells to IM.
