Nimbolide induces cell death in T lymphoma cells: Implication of altered apoptosis and glucose metabolism

2020 ◽  
Author(s):  
Pradip Kumar Jaiswara ◽  
Vishal Kumar Gupta ◽  
Pratishtha Sonker ◽  
Shiv Govind Rawat ◽  
Rajan Kumar Tiwari ◽  
...  
Keyword(s):  
Cell Death ◽  
Glucose Metabolism ◽  
Lymphoma Cells ◽  
T Lymphoma Cells ◽  
T Lymphoma

scholarly journals Haploinsufficiency of C2GnT-I glycosyltransferase renders T lymphoma cells resistant to cell death

Blood ◽  
2006 ◽  
Vol 108 (7) ◽  
pp. 2399-2406 ◽  
Author(s):  
Paula V. Cabrera ◽  
Maho Amano ◽  
Junya Mitoma ◽  
Jessica Chan ◽  
Jonathan Said ◽  
...  
Keyword(s):  
Cell Death ◽  
Dominant Negative ◽  
Mutant Enzyme ◽  
Dominant Negative Effect ◽  
Wild Type ◽  
Lymphoma Cells ◽  
T Lymphoma Cells ◽  
Negative Effect ◽  
T Lymphoma ◽  
Altered Cell

Abstract Neoplastic T cells in mycosis fungoides (MF) are resistant to apoptotic agents, including galectin-1 that is abundant in skin. Although MF cells are typically CD7–, and thus galectin-1 resistant, CD7+ HH cells, derived from a patient with MF, were also resistant to galectin-1. HH cells demonstrate altered cell surface glycosylation, with loss of core 2 O-glycan ligands for galectin-1 created by core 2 β1,6-N-acetylglucosaminyltransferase (C2GnT-I). Loss of core 2 O-glycans on tumor cells was also seen in primary CD7+ MF lesions. Surprisingly, HH cells are heterozygous for a C2GnT-I point mutation, yet this mutation resulted in a dramatic reduction in cellular glycosyltransferase activity. Expression of wild-type C2GnT-I in human HH cells, or murine lymphoma cells that lack C2GnT-I, restored core 2 O-glycan expression and susceptibility to galectin-1, whereas mutant enzyme lacked activity and did not restore core 2 O-glycan expression or susceptibility to galectin-1. Mutant enzyme did not have a dominant negative effect by affecting dimerization or activity of wild-type enzyme; rather, C2GnT-I haploinsufficiency is sufficient for loss of core 2 O-glycan expression and galectin-1 resistance. Thus, glycosyltransferase haploinsufficiency results in altered cellular glycosylation and resistance to cell death, identifying a new survival mechanism for T-lymphoma cells.

Lysophosphatidic acid promotes survival of T lymphoma cells by altering apoptosis and glucose metabolism

APOPTOSIS ◽  
2019 ◽  
Vol 25 (1-2) ◽  
pp. 135-150 ◽  
Author(s):  
Vishal Kumar Gupta ◽  
Pradip Kumar Jaiswara ◽  
Pratishtha Sonker ◽  
Shiv Govind Rawat ◽  
Rajan Kumar Tiwari ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Lysophosphatidic Acid ◽  
Lymphoma Cells ◽  
T Lymphoma Cells ◽  
T Lymphoma

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

scholarly journals Ryanodine Receptor-Ankyrin Interaction Regulates Internal Ca Release in Mouse T-lymphoma Cells

1995 ◽  
Vol 270 (30) ◽  
pp. 17917-17922 ◽  
Author(s):  
Lilly Y. W. Bourguignon ◽  
Arthur Chu ◽  
H. Jin ◽  
Neil R. Brandt
Keyword(s):  
Ryanodine Receptor ◽  
Lymphoma Cells ◽  
T Lymphoma Cells ◽  
T Lymphoma
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