scholarly journals Correction: Establishment and Characterization of PCL12, a Novel CD5+ Chronic Lymphocytic Leukaemia Cell Line

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0134748
Author(s):  
Andreas Agathangelidis ◽  
Lydia Scarfò ◽  
Federica Barbaglio ◽  
Benedetta Apollonio ◽  
Maria Teresa Sabrina Bertilaccio ◽  
...  
PLoS ONE ◽  
2015 ◽  
Vol 10 (6) ◽  
pp. e0130195 ◽  
Author(s):  
Andreas Agathangelidis ◽  
Lydia Scarfò ◽  
Federica Barbaglio ◽  
Benedetta Apollonio ◽  
Maria Teresa Sabrina Bertilaccio ◽  
...  

1999 ◽  
Vol 340 (2) ◽  
pp. 371-375 ◽  
Author(s):  
Kaushik DATTA ◽  
Shyam S. BISWAL ◽  
James P. KEHRER

The ability of various inhibitors of lipoxygenase (LOX) enzymes and 5-lipoxygenase-activating protein (FLAP) to induce apoptosis has implicated these pathways in the mechanism(s) of this form of cell death. Although FLAP plays an important role in 5-LOX activity, this protein is found at high levels in some cells lacking LOX, suggesting it might mediate other effects. Furthermore, the concentration of MK886, a FLAP inhibitor, required to induce apoptosis is ≈ 100-fold more than that required to inhibit LOX, and this compound remains effective in cells lacking LOX. The present study examines the role of FLAP in MK886-induced apoptosis. MK886 induced apoptosis in WSU cells, a human chronic lymphocytic leukaemia cell line that lacks FLAP protein and mRNA, suggesting that this agent is acting independently of FLAP. This conclusion was further supported by the fact that a more specific FLAP inhibitor, MK591, induced only minimal apoptosis in FL5.12 cells, a murine prolymphoid cell line containing FLAP. The role of FLAP was examined more directly by decreasing its expression by more than 50% in FL5.12 cells treated with 10 μM of an antisense oligonucleotide for 48 h. This change in FLAP was not accompanied by any increase in apoptosis. Furthermore, FLAP-depleted cells exhibited the same level of apoptosis 8 h after treatment with 10 μM MK886, as did control cells. The increased fluorescence seen in MK886-treated cells loaded with carboxydichlorofluorescein indicates that oxidative reactions are stimulated by this compound, possibly via the release of fatty acids from fatty acid-binding proteins and their subsequent oxidation.


1987 ◽  
Vol 11 (7) ◽  
pp. 579-588 ◽  
Author(s):  
Federico Caligaris-Cappio ◽  
Luciana Bergui ◽  
Giovanna Rege-Cambrin ◽  
Luisa Tesio ◽  
Nicola Migone ◽  
...  

2000 ◽  
Vol 109 (2) ◽  
pp. 396-404 ◽  
Author(s):  
Roland Walter ◽  
Gabriele Schoedon ◽  
Esther Bächli ◽  
David R. Betts ◽  
Johann P. Hossle ◽  
...  

2018 ◽  
Vol 22 (7) ◽  
pp. 3548-3559 ◽  
Author(s):  
Emilia Białopiotrowicz ◽  
Patryk Górniak ◽  
Monika Noyszewska‐Kania ◽  
Bartosz Puła ◽  
Hanna Makuch‐Łasica ◽  
...  

2020 ◽  
Vol 15 (3) ◽  
pp. 209-215
Author(s):  
Luka Horvat ◽  
Mariastefania Antica ◽  
Maja Matulić

Background:: Casein Kinase 2 (CK2) is a Ser/Thr protein kinase that coregulates a great number of signalling pathways in the cell. It is involved in cell cycle regulation and cell proliferation, apoptosis, DNA damage response and gene transcription. Its substrates are numerous kinases and transcription factors. It was found to be upregulated in different tumours, and certain types of leukaemia are very sensitive to its inhibition. Objective:: We analysed the effects of casein kinase 2 inhibition on three leukaemia cell lines of B and T cell origin: Jurkat, a T cell line, CLL, a chronic B lymphocytic leukaemia cell line and 697, a pre-B acute lymphocytic leukaemia cell line. Besides cell proliferation and cytotoxicity analysis, the aim was to investigate the influence of CK2 inhibition on elements of the Notch signalling pathway. Notch signalling has an important role in blood cell differentiation, and CK2 regulates Ikaros, a tumour suppressor interfering with Notch signalling Methods:: and T leukaemia cells were treated with different concentrations of the CK2 inhibitor, CX-4945, for 6 days, and cell viability and proliferation were determined by Trypan Blue Exclusion Method. Analysis of gene expression was performed by RT-qPCR. Results:: All three cell lines were sensitive to CK2 inhibition and among them, 697 cells had two times lower IC50. In Jurkat and CLL cells changes in c-Myc and Notch pathway gene expression were found. Conclusion:: As CK2 is involved in numerous signalling circuits, we concluded that each cell type could have a cell-specific response in gene expression.


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