Paclitaxel (Taxol®)-induced apoptosis in human epithelioid sarcoma cell lines is enhanced by upregulation of CD95 ligand (FasL/Apo-1L)

2007 ◽  
Vol 134 (6) ◽  
pp. 689-695 ◽  
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Sebastian Heikaus ◽  
Krystian S. Matuszek ◽  
Christoph V. Suschek ◽  
Uwe Ramp ◽  
Petra Reinecke ◽  
...  
2015 ◽  
Vol 238 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Farzad Jamshidi ◽  
Ali Bashashati ◽  
Karey Shumansky ◽  
Brendan Dickson ◽  
Nalan Gokgoz ◽  
...  

2001 ◽  
Vol 37 ◽  
pp. S111
Author(s):  
Sandra Tomek ◽  
Wolfgang Koestler ◽  
Thomas Brodowicz ◽  
Ingrid Pribill ◽  
Alexandra Budinsky ◽  
...  

1995 ◽  
Vol 121 (S1) ◽  
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R. Engers ◽  
C. D. Gerharz ◽  
R. Krause-Paulus ◽  
N. El-Badawy ◽  
...  

2000 ◽  
Vol 36 (9) ◽  
pp. 1171-1179 ◽  
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C.-D. Gerharz ◽  
U. Ramp ◽  
P. Reinecke ◽  
C. Schardt ◽  
U. Friebe ◽  
...  

2003 ◽  
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W Koestler ◽  
P Horak ◽  
T Grunt ◽  
T Brodowicz ◽  
...  

Author(s):  
D. W. Fairbain ◽  
M.D. Standing ◽  
K.L. O'Neill

Apoptosis is a genetically defined response to physiological stimuli that results in cellular suicide. Features common to apoptotic cells include chromatin condensation, oligonucleosomal DNA fragmentation, membrane blebbing, nuclear destruction, and late loss of ability to exclude vital dyes. These characteristics contrast markedly from pathological necrosis, in which membrane integrity loss is demonstrated early, and other features of apoptosis, which allow a non-inflammatory removal of dead and dying cells, are absent. Using heat shock-induced apoptosis as a model for examining stress response in cells, we undertook to categorize a variety of human leukemias and lymphomas with regard to their response to heat shock. We were also interested in determining whether a common temporal order was followed in cells dying by apoptosis. In addition, based on our previous results, we investigated whether increasing heat load resulted in increased apoptosis, with particular interest in relatively resistant cell lines, or whether the mode of death changed from apoptosis to necrosis.


Author(s):  
Paola Castillo-Juárez ◽  
Sebastián C. Sanchez ◽  
Alma D. Chávez-Blanco ◽  
Humberto Mendoza-Figueroa ◽  
José Correa-Basurto

Background and Objective: Histone deacetylases (HDACs) are important therapeutic targets for many types of human cancers. A derivative of valproic acid, N-(2-hydroxyphenyl)-2-propylpentanamide (HO-AAVPA), has antiproliferative properties on some cancer cell lines and inhibits the HDAC1 isoform. Materials and Methods: In this work, HO-AAVPA was tested as an antiproliferative agent in U87-MG (human glioblastoma) and U-2 OS cells (human osteosarcoma), which are types of cancer that are difficult to treat, and its antiangiogenic properties were explored. Results: HO-AAVPA had antiproliferative effects at 48 h with an IC50 = 0.655 mM in U87-MG cells and an IC50 = 0.453 mM in U-2 OS cells. Additionally, in the colony formation assay, HO-AAVPA decreased the number of colonies by approximately 99% in both cell lines and induced apoptosis by 31.3% in the U-2 OS cell line and by 78.2% in the U87-MG cell line. Additionally, HO-AAVPA reduced the number of vessels in chorioallantoid membranes (CAMs) by approximately 67.74% and IL-6 levels in both cell lines suggesting that the biochemical mechanism on cancer cell of HO-AAVPA is different compared to VPA. Conclusion: HO-AAVPA has antiproliferative effects on glioblastoma and osteosarcoma and antiangiogenic properties.


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