|
|
The effect of copper metabolism domain containing 1 in U87 cells proliferation and apoptosis and mechanism study |
RUAN Dong1 GUO Lirui2 WANG Fang2 YUAN Fan′en2 CHEN Qianxue2 LIU Baohui2 |
1.Department of Neurological Surgery, the First Affiliated Hospital of Hubei University of Science and Technology Xianning Central Hospital, Hubei Province, Xianning 437100, China;
2.Department of Neurological Surgery, Renmin Hospital of Wuhan University, Hubei Province, Wuhan 430060, China |
|
|
Abstract [Abstract] Objective To study the biological function of copper metabolism domain containing 1(COMMD1) in glioma cells U87 and its mechanism. Methods siRNA transfection was applied to knock down COMMD1 expression in U87 cells. CCK-8 and flow cytometry analysis were employed to examine glioma cells proliferation and apoptosis after COMMD1 was knocked down. Western blot was used to detect the expression of p65, cleaveage-caspase3 and BAD levels. Results Data showed that when COMMD1 was knocked down by siCOMMD1, the CCK8 results of siCOMMD1 were (0.402±0.000), (0.510±0.001), (1.021±0.002), (1.612±0.002), while the CCK8 results of siNC were (0.401±0.001), (0.452±0.002), (0.621±0.002), (0.823±0.003) at 0, 1, 2, 3 d; there were significantly differences in cell viabilities between the two group at 2 d and 3 d (P < 0.05). Flow cytometry analysis results showed that the apoptosis rate of cells in siCOMMD1 group and siNC group was (2.214±0.325)% and (7.121±0.520)%, there was significantly difference between the two group (P < 0.05). Western blot results showed that the expression of p65 and BAD increased 40.132% and 90.157%, cleaveage-caspase3 decreased 56.169% when COMMD1 was knocked down. Conclusion COMMD1 can regulate U87 cells apoptosis and proliferation.
|
|
|
|
|
[1] Lam FC,Yaffe MB. Kicking Genomic Profiling to the Curb:How Re-wiring the Phosphoproteome Can Explain Treatment Resistance in Glioma [J]. Cancer Cell,2016,29(4):435-436.
[2] Ramaswamy V,Taylor MD. Fall of the Optical Wall:Freedom from the Tyranny of the Microscope Improves Glioma Risk Stratification [J]. Cancer Cell,2016,29(2):137-138.
[3] Ho VK,Reijneveld JC,Enting RH,et al. Changing incidence and improved survival of gliomas [J]. Eur J Cancer,2014,50(13):2309-2318.
[4] Omuro A,DeAngelis LM. Glioblastoma and other malignant gliomas:a clinical review [J]. JAMA,2013,310(17):1842-1850.
[5] Ellis HP,Greenslade M,Powell B,et al. Current Challenges in Glioblastoma:Intratumour Heterogeneity,Residual Disease,and Models to Predict Disease Recurrence [J]. Front Oncol,2015,5:251.
[6] Wang Q,Hu B,Hu X,et al. Tumor Evolution of Glioma-Intrinsic Gene Expression Subtypes Associates with Immunological Changes in the Microenvironment [J]. Cancer Cell,2017,32(1):42-56.
[7] Nagaraja S,Vitanza NA,Woo PJ,et al. Transcriptional Dependencies in Diffuse Intrinsic Pontine Glioma [J]. Cancer Cell,2017,31(5):635-652.
[8] Lin X,Liu B,Yang X,et al. Genetic deletion of Rnd3 results in aqueductal stenosis leading to hydrocephalus through up-regulation of Notch signaling [J]. Proc Natl Acad Sci U S A,2013,110(20):8236-8341.
[9] Liu B,Lin X,Yang X,et al. Downregulation of RND3/RhoE in glioblastoma patients promotes tumorigenesis through augmentation of notch transcriptional complex activity [J]. Cancer Med,2015,4(9):1404-1416.
[10] Liu B,Dong H,Lin X,et al. RND3 promotes Snail 1 protein degradation and inhibits glioblastoma cell migration and invasion [J]. Oncotarget,2016,7(50):82411-82423.
[11] 陈奇钻,郭振涛,刘宝辉,等.RhoE基因对胶质瘤凋亡的影响及其机制[J].中华实验外科杂志,2013,30(9):104-109.
[12] Barresi V,Trovato-Salinaro A,Spampinato G,et al. Transcriptome analysis of copper homeostasis genes reveals coordinated upregulation of SLC31A1,SCO1,and COX11 in colorectal cance [J]. FEBS Open Bio,2016,6(8):794-806.
[13] Yeh DW,Chen YS,Lai CY,et al. Downregulation of COMMD1 by miR-205 promotes a positive feedback loop for amplifying inflammatory- and stemness-associated properties of cancer cells [J]. Cell Death Differ,2016,23(5):841-852.
[14] Xu H,You M,Shi H,et al. Ubiquitin-mediated NFkappaB degradation pathway [J]. Cell Mol Immunol,2015,12(6):653-655.
[15] Thoms HC,Loveridge CJ,Simpson J,et al. Nucleolar targeting of RelA(p65) is regulated by COMMD1-dependent ubiquitination [J]. Cancer Res,2010,70(1):139-149.
[16] Taskinen M,Louhimo R,Koivula S,et al. Deregulation of COMMD1 is associated with poor prognosis in diffuse large B-cell lymphoma [J]. PLoS One,2014,9(3):e91031.
[17] 林哲绚,韩溟.肝细胞肝癌COMMD1的表达及其意义[J].现代肿瘤医学,2012,20(8):1640-1642.
[18] Mu P,Akashi T,Lu F,et al. A novel nuclear complex of DRR1,F-actin and COMMD1 involved in NF-kappaB degradation and cell growth suppression in neuroblas?鄄toma [J]. Oncogene,2017. doi:10.1038/onc.2017.181.
[19] Fedoseienko A,Wieringa HW,Wisman GB,et al. Nuclear COMMD1 Is Associated with Cisplatin Sensitivity in Ovarian Cancer [J]. PLoS One,2016,11(10):e0165385.
[20] 夏熙双,牛光明,陶胜忠,等.雷公藤红素联合顺铂对C6胶质瘤细胞凋亡作用的研究[J].中华老年医学杂志,2016,35(8):898-903.
[21] 付锴,江普查,宫睿,等.沉默高半胱氨酸蛋白61表达对人脑胶质瘤U-87MG细胞及其裸鼠移植瘤生长的抑制作用[J].中华实验外科杂志,2015,32(9):2081-2083.
[22] 秦丽娟,贾永森,赵喜庆,等.鸦胆子油乳注射液对胶质瘤细胞侵袭性的影响及其可能机制[J].四川大学学报:医学版,2016,47(3):321-324. |
|
|
|