Role of Di-allyl Disulfide, a Garlic Component in NF-κB Mediated Transient G2-M Phase Arrest and Apoptosis in Human Leukemic Cell-lines

2013 ◽  
Vol 65 (4) ◽  
pp. 611-622 ◽  
Author(s):  
Pritha Dasgupta ◽  
Sumita Sengupta (Bandyopadhyay)
Keyword(s):  
Cell Lines ◽  
Leukemic Cell ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines ◽  
Phase Arrest ◽  
M Phase

The role of iron in the growth of human leukemic cell lines

1984 ◽  
Vol 121 (1) ◽  
pp. 251-256 ◽  
Author(s):  
Monique Titeux ◽  
Ugo Testa ◽  
Fawzia Louache ◽  
Pierre Thomopoulos ◽  
Henri Rochant ◽  
...  
Keyword(s):  
Cell Lines ◽  
Leukemic Cell ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines

scholarly journals Unlike its Paralog LEDGF/p75, HRP-2 Is Dispensable for MLL-R Leukemogenesis but Important for Leukemic Cell Survival

Cells ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 192
Author(s):  
Siska Van Belle ◽  
Sara El Ashkar ◽  
Kateřina Čermáková ◽  
Filip Matthijssens ◽  
Steven Goossens ◽  
...  
Keyword(s):  
Growth Factor ◽  
Cell Survival ◽  
Cell Lines ◽  
Protein Interactions ◽  
Leukemic Cell ◽  
Related Protein ◽  
Histone Tails ◽  
Knockout Mouse Model ◽  
Leukemic Cell Lines

HDGF-related protein 2 (HRP-2) is a member of the Hepatoma-Derived Growth Factor-related protein family that harbors the structured PWWP and Integrase Binding Domain, known to associate with methylated histone tails or cellular and viral proteins, respectively. Interestingly, HRP-2 is a paralog of Lens Epithelium Derived Growth Factor p75 (LEDGF/p75), which is essential for MLL-rearranged (MLL-r) leukemia but dispensable for hematopoiesis. Sequel to these findings, we investigated the role of HRP-2 in hematopoiesis and MLL-r leukemia. Protein interactions were investigated by co-immunoprecipitation and validated using recombinant proteins in NMR. A systemic knockout mouse model was used to study normal hematopoiesis and MLL-ENL transformation upon the different HRP-2 genotypes. The role of HRP-2 in MLL-r and other leukemic, human cell lines was evaluated by lentiviral-mediated miRNA targeting HRP-2. We demonstrate that MLL and HRP-2 interact through a conserved interface, although this interaction proved less dependent on menin than the MLL-LEDGF/p75 interaction. The systemic HRP-2 knockout mice only revealed an increase in neutrophils in the peripheral blood, whereas the depletion of HRP-2 in leukemic cell lines and transformed primary murine cells resulted in reduced colony formation independently of MLL-rearrangements. In contrast, primary murine HRP-2 knockout cells were efficiently transformed by the MLL-ENL fusion, indicating that HRP-2, unlike LEDGF/p75, is dispensable for the transformation of MLL-ENL leukemogenesis but important for leukemic cell survival.

scholarly journals The effects of alkyl-lysophospholipids on leukemic cell lines. I. Differential action on two human leukemic cell lines, HL60 and K562

Blood ◽  
1981 ◽  
Vol 57 (4) ◽  
pp. 794-797 ◽  
Author(s):  
T Tidwell ◽  
G Guzman ◽  
WR Vogler
Keyword(s):  
Bone Marrow ◽  
Cell Lines ◽  
Leukemic Cell ◽  
Short Term ◽  
Cell Numbers ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines ◽  
Low Concentrations ◽  
Bone Marrow Cultures ◽  
Differential Action

Abstract The action of an alkyl-lysophospholipid (ALP), ET180CH3, on clonogenicity, 3H-TdR uptake, and cell numbers was tested in two human leukemic cell lines, HL60 and K562, and short-term human leukemic bone marrow cultures. ALP eliminated clonogenicity in HL60 but not in K562 cultures; 3H-TdR uptake and cell numbers were depressed at low concentrations of ET180CH3 in HL60, but not K562 cultures. The action of the lysophospholipid analog on human leukemic bone marrow short-term cultures at low concentrations was similar to its action on HL60 cultures; clonogenicity and 3H-TdR uptake were depressed, but cell numbers were not significantly affected. The demonstration of differential action of ALP on two cell lines should significantly simplify the investigation of the mechanism of the reported differential action of ET180CH3 on normal and leukemic cell membranes.

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