scholarly journals 4-Hydroxyderricin from Angelica keiskei Roots Induces Caspase-dependent Apoptotic Cell Death in HL60 Human Leukemia Cells

2011 ◽  
Vol 60 (2) ◽  
pp. 71-77 ◽  
Author(s):  
Toshihiro Akihisa ◽  
Takashi Kikuchi ◽  
Hisashi Nagai ◽  
Koichi Ishii ◽  
Keiichi Tabata ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Angelica Keiskei

Melatonin enhances hyperthermia-induced apoptotic cell death in human leukemia cells

2016 ◽  
Vol 61 (3) ◽  
pp. 381-395 ◽  
Author(s):  
Carlos Quintana ◽  
Javier Cabrera ◽  
Juan Perdomo ◽  
Francisco Estévez ◽  
Juan F. Loro ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells

scholarly journals UNBS1450, a steroid cardiac glycoside inducing apoptotic cell death in human leukemia cells

2011 ◽  
Vol 81 (1) ◽  
pp. 13-23 ◽  
Author(s):  
Tom Juncker ◽  
Claudia Cerella ◽  
Marie-Hélène Teiten ◽  
Franck Morceau ◽  
Marc Schumacher ◽  
...  
Keyword(s):  
Cell Death ◽  
Cardiac Glycoside ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells

Berberine Induces Apoptotic Cell Death via Activation of Caspase-3 and -8 in HL-60 Human Leukemia Cells: Nuclear Localization and Structure–Activity Relationships

2017 ◽  
Vol 45 (07) ◽  
pp. 1497-1511 ◽  
Author(s):  
Shinya Okubo ◽  
Takuhiro Uto ◽  
Aya Goto ◽  
Hiroyuki Tanaka ◽  
Tsuyoshi Nishioku ◽  
...  
Keyword(s):  
Cell Death ◽  
Dna Fragmentation ◽  
Antiproliferative Activity ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Leukemia Cells ◽  
Caspase 8 ◽  
Human Leukemia ◽  
Caspase 9

Berberine (BBR), an isoquinoline alkaloid, is a well-known bioactive compound contained in medicinal plants used in traditional and folk medicines. In this study, we investigated the subcellular localization and the apoptotic mechanisms of BBR were elucidated. First, we confirmed the incorporation of BBR into the cell visually. BBR showed antiproliferative activity and promptly localized to the nucleus from 5[Formula: see text]min to 15[Formula: see text]min after BBR treatment in HL-60 human promyelocytic leukemia cells. Next, we examined the antiproliferative activity of BBR (1) and its biosynthetically related compounds (2-7) in HL-60 cells. BBR exerted strongest antiproliferative activity among 1-7 and the results of structures and activity relation suggested that a methylenedioxyl group in ring A, an [Formula: see text]-alkyl group at C-9 position, and the frame of isoquinoline may be necessary for antiproliferative activity. Moreover, BBR showed the most potent antiproliferative activity in HL-60 cells among human cancer and normal cell lines tested. Next, we examined the effect of BBR on molecular events known as apoptosis induction. In HL-60 cells, BBR induced chromatin condensation and DNA fragmentation, and triggered the activation of PARP, caspase-3 and caspase-8 without the activation of caspase-9. BBR-induced DNA fragmentation was abolished by pretreatment with inhibitors against caspase-3 and caspase-8, but not against caspase-9. ERK and p38 were promptly phosphorylated after 15 min of BBR treatment, and this was correlated with time of localization to the nucleus of BBR. These results demonstrated that BBR translocated into nucleus immediately after treatments and induced apoptotic cell death by activation of caspase-3 and caspase-8.

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.

Inhibition of DNA-dependent protein kinase promotes ultrasound-induced cell death including apoptosis in human leukemia cells

2012 ◽  
Vol 322 (1) ◽  
pp. 107-112 ◽  
Author(s):  
Yukihiro Furusawa ◽  
Yoshisada Fujiwara ◽  
Mariame Ali Hassan ◽  
Yoshiaki Tabuchi ◽  
Akinori Morita ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Dependent Protein Kinase ◽  
Human Leukemia Cells ◽  
Dependent Protein
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