scholarly journals Fucoidan inhibits proliferation of the SKM-1 acute myeloid leukaemia cell line via the activation of apoptotic pathways and production of reactive oxygen species

2015 ◽  
Vol 12 (5) ◽  
pp. 6649-6655 ◽  
Author(s):  
CHUNMEI WEI ◽  
QING XIAO ◽  
XINGYI KUANG ◽  
TAO ZHANG ◽  
ZESONG YANG ◽  
...  
2017 ◽  
Vol 192 ◽  
pp. 27-34
Author(s):  
Virginie Driss ◽  
Frédéric Leprêtre ◽  
Isabelle Briche ◽  
Alexia Mopin ◽  
Céline Villenet ◽  
...  

PLoS ONE ◽  
2009 ◽  
Vol 4 (1) ◽  
pp. e4251 ◽  
Author(s):  
Stefano Tiziani ◽  
Alessia Lodi ◽  
Farhat L. Khanim ◽  
Mark R. Viant ◽  
Christopher M. Bunce ◽  
...  

2005 ◽  
Vol 115 (1-2) ◽  
pp. 109-114 ◽  
Author(s):  
Shane A. Olwill ◽  
Hugh McGlynn ◽  
William S. Gilmore ◽  
H. Denis Alexander

Author(s):  
Stefano Tiziani ◽  
Alessia Lodi ◽  
Farhat L. Khanim ◽  
Mark R. Viant ◽  
Christopher M. Bunce ◽  
...  

2021 ◽  
Author(s):  
Nuria Vilaplana-Lopera ◽  
Ruba Almaghrabi ◽  
Grigorios Papatzikas ◽  
Elena González ◽  
Alan Cunningham ◽  
...  

SummaryAcute myeloid leukaemia (AML) cells interact and modulate components of their surrounding microenvironment into their own benefit. Stromal cells have been shown to support AML survival and progression through various mechanisms. Nonetheless, it is unclear whether AML cells could establish beneficial metabolic interactions with stromal cells. Here, we identify a novel metabolic crosstalk between AML and stromal cells where AML cells prompt stromal cells to secrete acetate for their own consumption. By performing transcriptome analysis and tracer-based NMR studies, we show that stromal cells present a higher rate of glycolysis, and that the secreted acetate derives from pyruvate via a reactive oxygen species (ROS)-mediated process. Our data also reveals that AML cells transfer ROS to stromal cells using gap junctions. Overall, we present a unique metabolic communication between AML and stromal cells that could be exploited as adjuvant therapy.


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