Antitumor activity of 3?, 5?-diesters of 5-fluoro-2?-deoxyuridine against murine leukemia L1210 cells

1981 ◽  
Vol 6 (1) ◽  
Author(s):  
Fumihiko Kanzawa ◽  
Akio Hoshi ◽  
Kazuo Kuretani ◽  
Mineo Saneyoshi ◽  
Takeo Kawaguchi
1998 ◽  
Vol 110 (1) ◽  
pp. 79-83 ◽  
Author(s):  
Sally H. Ibbotson ◽  
Christopher R. Lambert ◽  
Michael N. Moran ◽  
Mary C. Lynch ◽  
Irene E. Kochevar

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Jai-Sing Yang ◽  
Chia-Chun Wu ◽  
Chao-Lin Kuo ◽  
Yu-Hsuan Lan ◽  
Chin-Chung Yeh ◽  
...  

We investigated the molecular mechanisms of cell cycle arrest and apoptotic death induced bySolanum lyratumextracts (SLE) or diosgenin in WEHI-3 murine leukemia cellsin vitroand antitumor activityin vivo. Diosgenin is one of the components of SLE. Our study showed that SLE and diosgenin decreased the viable WEHI-3 cells and inducedG0/G1phase arrest and apoptosis in concentration- or time-dependent manners. Both reagents increased the levels of ROS production and decreased the mitochondrial membrane potential (ΔΨm). SLE- and diosgenin-triggered apoptosis is mediated through modulating the extrinsic and intrinsic signaling pathways. Intriguingly, the p53 inhibitor (pifithrin-α), anti-Fas ligand (FasL) mAb, and specific inhibitors of caspase-8 (z-IETD-fmk), caspase-9 (z-LEHD-fmk), and caspase-3 (z-DEVD-fmk) blocked SLE- and diosgenin-reduced cell viability of WEHI-3 cells. Thein vivostudy demonstrated that SLE has marked antitumor efficacy against tumors in the WEHI-3 cell allograft model. In conclusion, SLE- and diosgenin-inducedG0/G1phase arrest and triggered extrinsic and intrinsic apoptotic pathways via p53 activation in WEHI-3 cells. SLE also exhibited antitumor activityin vivo. Our findings showed that SLE may be potentially efficacious in the treatment of leukemia in the future.


Cytometry ◽  
2003 ◽  
Vol 56A (2) ◽  
pp. 89-95 ◽  
Author(s):  
R. O. Bilyy ◽  
R. S. Stoika
Keyword(s):  

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