Abstract 4621: The histone methyltransferase EZH2 catalytic activity is required for cell growth in diffuse large B-cell lymphoma.

2013 ◽  
Author(s):  
James E. Audia ◽  
Patrick Trojer ◽  
Shivani Garapaty ◽  
Fei Lan ◽  
Vidya Balasubramanian ◽  
...  
Keyword(s):  
Catalytic Activity ◽  
Cell Growth ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Histone Methyltransferase ◽  
Large B Cell Lymphoma ◽  
Large B Cell

541 The Histone Methyltransferase EZH2 is Required for Cell Growth in Diffuse Large B-cell Lymphoma

2012 ◽  
Vol 48 ◽  
pp. 166-167
Author(s):  
P. Trojer ◽  
S. Garapaty ◽  
F. Lan ◽  
V. Balsubramanian ◽  
E. Chan ◽  
...  
Keyword(s):  
Cell Growth ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Histone Methyltransferase ◽  
Large B Cell Lymphoma ◽  
Large B Cell

scholarly journals PMA/IONO affects diffuse large B-cell lymphoma cell growth through upregulation of A20 expression

2016 ◽  
Vol 36 (2) ◽  
pp. 1069-1075 ◽  
Author(s):  
Wenxiu Yang ◽  
Yi Li ◽  
Pinhao Li ◽  
Lingling Wang
Keyword(s):  
Cell Growth ◽  
B Cell ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Lymphoma Cell ◽  
Large B Cell Lymphoma ◽  
Large B Cell

scholarly journals Acetylshikonin Suppresses Diffuse Large B-Cell Lymphoma Cell Growth By Targeting The TOPK Signaling Pathway

2021 ◽  
Author(s):  
Jieke Cui ◽  
Rong Guo ◽  
Yingjun Wang ◽  
Yue Song ◽  
Xuewen Song ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Cell Growth ◽  
Western Blot ◽  
B Cell ◽  
Blot Analysis ◽  
Western Blot Analysis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Abstract Background: Diffuse large B-cell lymphoma (DLBCL) is one of the most common causes of cancer death worldwide, and responds badly to the existing treatment. Thus, identifying the novel therapeutic targets of DLBCL are urgent. Methods and results: In this study, we found that the T-lymphokine-activated killer cell-originated protein kinase (TOPK) was highly expressed in DLBCL cells and tissues. The TOPK expression were analyzed by bioinformatics analysis, immunohistochemistry (IHC) and western blot analysis. TOPK knockdown inhibited cell growth and induced apoptosis of DLBCL cells with MTS and flow cytometry. Further experiments demonstrated that acetylshikonin, the targeted compound of TOPK, could attenuate the cell growth and aggravate the cell apoptosis through TOPK/extra cellular signal-regulated kinase (ERK)-1/2 signaling using MTS, flow cytometry and western blot analysis. In addition, we demonstrated that TOPK overexpression significantly reduced the acetylshikonin effect on cell proliferation and apoptosis in U2932 and OCI-LY8 cells using MTS, flow cytometry and western blot analysis. Conclusions: Taken together, the present study suggests that the targeted inhibition of TOPK by acetylshikonin may be a promising approach to the treatment of DLBCL.

scholarly journals Matrine suppresses cell growth of diffuse large B-cell lymphoma via inhibiting CaMKIIγ/c-Myc/CDK6 signaling pathway

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Jianyou Gu ◽  
Xiao Wang ◽  
Ling Zhang ◽  
Jingjing Xiang ◽  
Jingya Li ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Growth ◽  
B Cell ◽  
Signaling Pathway ◽  
Cell Lymphoma ◽  
Ectopic Expression ◽  
B Cell Lymphoma ◽  
Dependent Manner ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Abstract Background C-Myc aberrations confer a more aggressive clinic behavior in diffuse large B-cell lymphoma (DLBCL). Matrine is an alkaloid extracted from Sophora flavescens Ait. It possesses anti-cancer property through inhibiting the cell proliferation and inducing the apoptosis. The present study aimed to explore the underlying mechanisms of matrine in suppressing the cell growth of DLBCL. Methods The influence of matrine on the viability of cultured DLBCL cell lines SU-DHL-16 and OCI-LY3 cells were determined by CCK-8. Apoptosis and cell cycle were measured by flow cytometry after matrine exposure. Western blot was taken to investigate the expression of activated Caspase-3, cleaved PARP, c-Myc, phospho-c-Myc (Ser62), CaMKIIγ, phospho-CaMKIIγ (Thr287), CDK4 and CDK6 after matrine treatment. Cycloheximide chase analysis was used to determine the c-Myc protein half-lives before and after matrine treatment. Growth salvage analysis was taken by ectopic expression of c-Myc. Results In cultured DLBCL cells, matrine suppressed cell viability in a concentration and time dependent fashion. Matrine treated SU-DHL-16 and OCI-LY3 cells for 48 h with IC50 value of 1.76 mM and 4.1 mM, respectively. Matrine induced apoptosis through a caspase-independent pathway and caused G0/G1 cell cycle arrest in a concentration dependent manner in DLBCL cells. The protein expression of c-Myc was inhibited while the transcription of c-Myc was not reduced by matrine. c-Myc protein half-lives were decreased from 30.4, 69.4 min to 16.6, 15.9 min after matrine treatment in SU-DHL-16 and OCI-LY3, respectively. As a critical protein kinase of c-Myc, CaMKIIγ phosphorylation at Thr287 was found to be down-regulated and c-Myc phosphorylation at Ser62 was reduced together after matrine treatment in DLBCL. The growth suppression of SU-DHL-16 cells induced by matrine was rescued by over-expression of c-Myc achieved by recombinant adenovirus infection. The decreased expression of CDK6, not CDK4, induced by matrine was rescued by ectopic expression of c-Myc protein. Conclusions This study has shown for the first time that matrine suppresses cell growth of DLBCL via inhibiting CaMKIIγ/c-Myc/CDK6 signaling pathway.

ASPM predicts poor clinical outcome and promotes tumorigenesis for diffuse large B-cell lymphoma

2020 ◽  
Vol 20 ◽  
Author(s):  
Jingjing Wu ◽  
Zhengmei He ◽  
Yaning Zhu ◽  
Chao Jiang ◽  
Yuan Deng ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Overall Survival ◽  
Cell Growth ◽  
B Cell ◽  
Cell Apoptosis ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Reactive Lymphoid Hyperplasia ◽  
Large B Cell Lymphoma ◽  
Large B Cell

Background: Abnormal spindle-like microcephaly-associated protein (ASPM) has been implicated in the aggressive behavior of several malignant tumors. However, its potential effects on diffuse large B-cell lymphoma (DLBCL) still remain unknown. Method: ASPM levels were determined by immunohistochemically in DLBCL tissues from 54 patients treated with CHOP or R-CHOP regimen and 15 reactive lymphoid hyperplasia (RLH) tissues as control, and its association with clinical features and overall survival were evaluated. The effects of ASPM on cell growth, cell apoptosis and cell cycle of DLBCL cells were assessed. Bioinformatics, quantitative RT-PCR and western blotting were conducted for mechanic investigation. Results: ASPM expression was upregulated in DLBCL tissues compared with RLH tissues. Its high expression was correlated with inferior clinicopathological characteristics and poor overall survival of DLBCL patients. Multivariate analysis revealed that high ASPM expression emerged as an independent factor for poor prognosis. In DLBCL cell lines, silencing of ASPM suppressed cell growth, induced cell apoptosis and arrested the cell cycle. Mechanically, the effects of ASPM knockdown on DLBCL cells were partially dependent on its block of the Wnt/β-catenin pathway. Conclusion: Collectively, our results suggested that ASPM potentially served as a predictive biomarker of DLCBL tumorigenesis and prognosis, representing a potential therapeutic target for DLCBL.

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