scholarly journals The p27–Skp2 axis mediates glucocorticoid-induced cell cycle arrest in T-lymphoma cells

Cell Cycle ◽  
2013 ◽  
Vol 12 (16) ◽  
pp. 2625-2635 ◽  
Author(s):  
Michael K Kullmann ◽  
Claudia Grubbauer ◽  
Katrin Goetsch ◽  
Heidelinde Jäkel ◽  
Silvio R Podmirseg ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Lymphoma Cells ◽  
Cycle Arrest ◽  
T Lymphoma Cells ◽  
T Lymphoma

UVA-activated 8-methoxypsoralen (PUVA) causes G2/M cell cycle arrest in Karpas 299 T-lymphoma cells

2006 ◽  
Vol 85 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Jitka Bartošová ◽  
Kateřina Kuželová ◽  
Michaela Pluskalová ◽  
Iuri Marinov ◽  
Petr Halada ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
M Cell ◽  
Lymphoma Cells ◽  
Cycle Arrest ◽  
T Lymphoma Cells ◽  
T Lymphoma

DNA damage-induced [Zn2+]i transients: correlation with cell cycle arrest and apoptosis in lymphoma cells

2002 ◽  
Vol 283 (2) ◽  
pp. C609-C622 ◽  
Author(s):  
Paul J. Smith ◽  
Marie Wiltshire ◽  
Sharon Davies ◽  
Suet-Feung Chin ◽  
Anthony K. Campbell ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Stress Responses ◽  
Damage Threshold ◽  
Lymphoma Cells ◽  
Cycle Arrest ◽  
Competent Cells ◽  
Drug Doses ◽  
Induced Apoptosis

Reactive changes in free intracellular zinc cation concentration ([Zn2+]i) were monitored, using the fluorescent probe Zinquin, in human lymphoma cells exposed to the DNA-damaging agent VP-16. Two-photon excitation microscopy showed that Zinquin-Zn2+ forms complexes in cytoplasmic vesicles. [Zn2+]iincreased in both p53wt (wild type) and p53mut(mutant) cells after exposure to low drug doses. In p53mutcells noncompetent for DNA damage-induced apoptosis, elevated [Zn2+]i was maintained at higher drug doses, unlike competent p53wt cells that showed a collapse of the transient before apoptosis. In p53wt cells, the [Zn2+]i rise paralleled an increase in p53 and bax-to-bcl-2 ratio but preceded an increase in p21WAF1, active cell cycle arrest in G2, or nuclear fragmentation. Reducing [Zn2+]i, using N, N, N′, N′-tetrakis(2-pyridylmethyl)ethylenediamine, caused rapid apoptosis in both p53wt and p53mut cells, although cotreatment with VP-16 exacerbated apoptosis only in p53wt cells. This may reflect changed thresholds for proapoptotic caspase-3 activation in competent cells. We conclude that the DNA damage-induced transient is p53-independent up to a damage threshold, beyond which competent cells reduce [Zn2+]i before apoptosis. Early stress responses in p53wt cells take place in an environment of enhanced Zn2+ availability.

scholarly journals SYK inhibition and response prediction in diffuse large B-cell lymphoma

Blood ◽  
2011 ◽  
Vol 118 (24) ◽  
pp. 6342-6352 ◽  
Author(s):  
Shuhua Cheng ◽  
Greg Coffey ◽  
X. Hannah Zhang ◽  
Rita Shaknovich ◽  
Zibo Song ◽  
...  
Keyword(s):  
Cell Cycle ◽  
B Cell ◽  
Cell Cycle Arrest ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Lymphoma Cells ◽  
Cycle Arrest ◽  
Large B Cell Lymphoma ◽  
Bcr Signaling ◽  
Large B Cell

Abstract Diffuse large B-cell lymphoma (DLBCL) is the most common type of non-Hodgkin lymphoma, and the role of SYK in its pathogenesis is not completely understood. Using tissue microarray, we demonstrated for the first time that SYK protein is activated in 27 of 61 (44%) primary human DLBCL tissues. Among DLBCL cell lines, 7 were sensitive and 3 were resistant to a highly specific SYK inhibitor, PRT060318. In sensitive DLBCL cells, SYK inhibition blocked the G1-S transition and caused cell-cycle arrest. This effect was reproduced by genetic reduction of SYK using siRNA. A detailed analysis of the BCR signaling pathways revealed that the consequence of SYK inhibition on PLCγ2 and AKT, as opposed to ERK1/2, was responsible for cell-cycle arrest. Genetic knock-down of these key molecules decelerated the proliferation of lymphoma cells. In addition, BCR signaling can be blocked by PRT060318 in primary lymphoma cells. Together, these findings provide insights into cellular pathways required for lymphoma cell growth and support the rationale for considering SYK inhibition as a potentially useful therapy for DLBCL. The results further suggest the possibility of using PLCγ2 and AKT as biomarkers to predict therapeutic response in prospective clinical trials of specific SYK inhibitors.

scholarly journals Thyroid status modulates T lymphoma growth via cell cycle regulatory proteins and angiogenesis

2014 ◽  
Vol 222 (2) ◽  
pp. 243-255 ◽  
Author(s):  
H A Sterle ◽  
E Valli ◽  
F Cayrol ◽  
M A Paulazo ◽  
D J Martinel Lamas ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Tumor Suppressor ◽  
Solid Tumors ◽  
Regulatory Proteins ◽  
Thyroid Status ◽  
Lymphoma Cells ◽  
T Lymphoma Cells ◽  
Cell Cycle Regulatory Proteins ◽  
T Lymphoma

We have shownin vitrothat thyroid hormones (THs) regulate the balance between proliferation and apoptosis of T lymphoma cells. The effects of THs on tumor development have been studied, but the results are still controversial. Herein, we show the modulatory action of thyroid status on thein vivogrowth of T lymphoma cells. For this purpose, euthyroid, hypothyroid, and hyperthyroid mice received inoculations of EL4 cells to allow the development of solid tumors. Tumors in the hyperthyroid animals exhibited a higher growth rate, as evidenced by the early appearance of palpable solid tumors and the increased tumor volume. These results are consistent with the rate of cell division determined by staining tumor cells with carboxyfluorescein succinimidyl ester. Additionally, hyperthyroid mice exhibited reduced survival. Hypothyroid mice did not differ significantly from the euthyroid controls with respect to these parameters. Additionally, only tumors from hyperthyroid animals had increased expression levels of proliferating cell nuclear antigen and active caspase 3. Differential expression of cell cycle regulatory proteins was also observed. The levels of cyclins D1 and D3 were augmented in the tumors of the hyperthyroid animals, whereas the cell cycle inhibitors p16/INK4A (CDKN2A) and p27/Kip1 (CDKN1B) and the tumor suppressor p53 (TRP53) were increased in hypothyroid mice. Intratumoral and peritumoral vasculogenesis was increased only in hyperthyroid mice. Therefore, we propose that the thyroid status modulates thein vivogrowth of EL4 T lymphoma through the regulation of cyclin, cyclin-dependent kinase inhibitor, and tumor suppressor gene expression, as well as the stimulation of angiogenesis.

Catfish rhamnose-binding lectin induces G0/1 cell cycle arrest in Burkitt’s lymphoma cells via membrane surface Gb3

2016 ◽  
Vol 34 (1) ◽  
pp. 127-138 ◽  
Author(s):  
Shigeki Sugawara ◽  
Changhun Im ◽  
Tasuku Kawano ◽  
Takeo Tatsuta ◽  
Yasuhiro Koide ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Arrest ◽  
Membrane Surface ◽  
Burkitt’S Lymphoma ◽  
Burkitt's Lymphoma ◽  
Lymphoma Cells ◽  
Cycle Arrest ◽  
Binding Lectin ◽  
Burkitt’S Lymphoma Cells
Sign in / Sign up

Export Citation Format

Share Document