scholarly journals Dephosphorylation and mitochondrial translocation of cofilin sensitizes human leukemia cells to cerulenin-induced apoptosis via the ROCK1/Akt/JNK signaling pathway

Oncotarget ◽  
2016 ◽  
Vol 7 (15) ◽  
pp. 20655-20668 ◽  
Author(s):  
Yanhao Zhang ◽  
Ruoqiu Fu ◽  
Yanxia Liu ◽  
Jing Li ◽  
Hongwei Zhang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Jnk Signaling ◽  
Mitochondrial Translocation ◽  
Human Leukemia Cells ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis

scholarly journals Phloretin-induced Apoptosis in B16 Melanoma 4A5 Cells and HL60 Human Leukemia Cells

1999 ◽  
Vol 63 (4) ◽  
pp. 719-725 ◽  
Author(s):  
Masuko KOBORI ◽  
Keiko IWASHITA ◽  
Hiroshi SHINMOTO ◽  
Tojiro TSUSHIDA
Keyword(s):  
B16 Melanoma ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Induced Apoptosis

Mechanism of patulin-induced apoptosis in human leukemia cells (HL-60)

2008 ◽  
Vol 183 (1-3) ◽  
pp. 105-111 ◽  
Author(s):  
T WU ◽  
Y LIAO ◽  
F YU ◽  
C CHANG ◽  
B LIU
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Induced Apoptosis

scholarly journals 1-Cinnamoyltrichilinin from Melia azedarach Causes Apoptosis through the p38 MAPK Pathway in HL-60 Human Leukemia Cells

2020 ◽  
Vol 21 (20) ◽  
pp. 7506
Author(s):  
Hoibin Jeong ◽  
SeonJu Park ◽  
Seo-Young Kim ◽  
Su-Hyeon Cho ◽  
Myeong Seon Jeong ◽  
...  
Keyword(s):  
Mapk Pathway ◽  
Leukemia Cells ◽  
Therapeutic Window ◽  
Melia Azedarach ◽  
Human Leukemia ◽  
Dependent Manner ◽  
P38 Inhibitor ◽  
Human Leukemia Cells ◽  
Induced Apoptosis ◽  
P38 Pathway

Acute myeloid leukemia (AML) is an aggressive type of human leukemia with a low survival rate, and its complete remission remains challenging. Although chemotherapy is the first-line treatment of AML, it exerts toxicity in noncancerous cells when used in high doses, thus necessitating the development of novel compounds with a high therapeutic window. This study aimed to investigate the anticancer effects of several compounds derived from the fruits of Melia azedarach (a tree with medicinal properties). Among them, 1-cinnamoyltrichilinin (CT) was found to strongly suppress the viability of HL-60 human leukemia cells. CT treatment induced apoptosis and increased nuclear fragmentation and fractional DNA content in HL-60 cells in a dose-dependent manner. CT induced phosphorylation of p38 mitogen-activated protein kinases (p38), though not of c-Jun N-terminal kinase (JNK) and extracellular signal-regulated kinase (ERK), and activated Bcl-2 family proteins towards the proapoptosis and cleavage of caspase-3 and poly (ADP-ribose) polymerase. Both CT-mediated apoptosis and apoptotic protein expression were reversed by treatment with the p38 inhibitor, thereby indicating the p38 pathway to be critical in CT-stimulated apoptosis. The results collectively indicated CT to suppress HL-60 survival by activating the p38 pathway and inducing apoptosis, hence being a novel potential therapeutic agent for AML.

scholarly journals Naja atra Cardiotoxin 3 Elicits Autophagy and Apoptosis in U937 Human Leukemia Cells through the Ca2+/PP2A/AMPK Axis

Toxins ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 527 ◽  
Author(s):  
Jing-Ting Chiou ◽  
Yi-Jun Shi ◽  
Liang-Jun Wang ◽  
Chia-Hui Huang ◽  
Yuan-Chin Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Membrane Damage ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
U937 Cells ◽  
Cell Membrane Damage ◽  
Human Leukemia Cells ◽  
Phosphatase 2A ◽  
Induced Apoptosis ◽  
Naja Atra

Cardiotoxins (CTXs) are suggested to exert their cytotoxicity through cell membrane damage. Other studies show that penetration of CTXs into cells elicits mitochondrial fragmentation or lysosome disruption, leading to cell death. Considering the role of AMPK-activated protein kinase (AMPK) in mitochondrial biogenesis and lysosomal biogenesis, we aimed to investigate whether the AMPK-mediated pathway modulated Naja atra (Taiwan cobra) CTX3 cytotoxicity in U937 human leukemia cells. Our results showed that CTX3 induced autophagy and apoptosis in U937 cells, whereas autophagic inhibitors suppressed CTX3-induced apoptosis. CTX3 treatment elicited Ca2+-dependent degradation of the protein phosphatase 2A (PP2A) catalytic subunit (PP2Acα) and phosphorylation of AMPKα. Overexpression of PP2Acα mitigated the CTX3-induced AMPKα phosphorylation. CTX3-induced autophagy was via AMPK-mediated suppression of the Akt/mTOR pathway. Removal of Ca2+ or suppression of AMPKα phosphorylation inhibited the CTX3-induced cell death. CTX3 was unable to induce autophagy and apoptosis in U937 cells expressing constitutively active Akt. Met-modified CTX3 retained its membrane-perturbing activity, however, it did not induce AMPK activation and death of U937 cells. These results conclusively indicate that CTX3 induces autophagy and apoptosis in U937 cells via the Ca2+/PP2A/AMPK axis, and suggest that the membrane-perturbing activity of CTX3 is not crucial for the cell death signaling pathway induction.

The role of the stress-activated protein kinase (SAPK/JNK) signaling pathway in radiation-induced apoptosis

1998 ◽  
Vol 47 (3) ◽  
pp. 225-232 ◽  
Author(s):  
Marcel Verheij ◽  
Gerald A Ruiter ◽  
Shuraila F Zerp ◽  
Wim J van Blitterswijk ◽  
Zvi Fuks ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Signaling Pathway ◽  
Jnk Signaling ◽  
Radiation Induced ◽  
Jnk Signaling Pathway ◽  
Induced Apoptosis
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