Induction of apoptotic cell death by direct-current treatment in human leukemic cell lines

1997 ◽  
Vol 123 (7) ◽  
pp. 370-376 ◽  
Author(s):  
Masatsugu Kurokawa ◽  
Hiroshi Sakagami ◽  
Fumio Kokubu ◽  
Hiromichi Noda ◽  
Minoru Takeda ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Direct Current ◽  
Apoptotic Cell ◽  
Leukemic Cell ◽  
Current Treatment ◽  
Apoptotic Cell Death ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines

Induction of apoptotic cell death by direct-current treatment in human leukemic cell lines

1997 ◽  
Vol 123 (7) ◽  
pp. 370-376 ◽  
Author(s):  
Masatsugu Kurokawa ◽  
Hiroshi Sakagami ◽  
Fumio Kokubu ◽  
Hiromichi Noda ◽  
Minoru Takeda ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Direct Current ◽  
Apoptotic Cell ◽  
Leukemic Cell ◽  
Current Treatment ◽  
Apoptotic Cell Death ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines

scholarly journals Greensporone A, a Fungal Secondary Metabolite Suppressed Constitutively Activated AKT via ROS Generation and Induced Apoptosis in Leukemic Cell Lines

Biomolecules ◽  
2019 ◽  
Vol 9 (4) ◽  
pp. 126 ◽  
Author(s):  
Kirti Prabhu ◽  
Kodappully Siveen ◽  
Shilpa Kuttikrishnan ◽  
Anh Jochebeth ◽  
Tayyiba Ali ◽  
...  
Keyword(s):  
Cell Death ◽  
Cytochrome C ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Leukemic Cell ◽  
Apoptotic Cell Death ◽  
Leukemic Cells ◽  
Leukemic Cell Lines ◽  
Fungal Secondary Metabolite

Greensporone A is a fungal secondary metabolite that has exhibited potential in vitro for anti-proliferative activity in vitro. We studied the anticancer activity of greensporone A in a panel of leukemic cell lines. Greensporone A-mediated inhibition of proliferation is found to be associated with the induction of apoptotic cell death. Greensporone A treatment of leukemic cells causes inactivation of constitutively activated AKT and its downstream targets, including members GSK3 and FOXO1, and causes downregulation of antiapoptotic genes such as Inhibitor of Apoptosis (IAPs) and Bcl-2. Furthermore, Bax, a proapoptotic member of the Bcl-2 family, was found to be upregulated in leukemic cell lines treated with greensporone A. Interestingly, gene silencing of AKT using AKT specific siRNA suppressed the expression of Bcl-2 with enhanced expression of Bax. Greensporone A-mediated increase in Bax/Bcl-2 ratio causes permeabilization of the mitochondrial membrane leading to the accumulation of cytochrome c in the cytoplasm. Greensporone A-induced cytochrome c accumulation causes the activation of caspase cascade and cleavage of its effector, poly(ADP-ribose) polymerase (PARP), leading to apoptosis. Greensporone A-mediated apoptosis in leukemic cells occurs through the generation of reactive oxygen species (ROS) due to depletion of glutathione (GSH) levels. Finally, greensporone A potentiated the anticancer activity of imatinib in leukemic cells. In summary, our study showed that greensporone A suppressed the growth of leukemic cells via induction of apoptotic cell death. The apoptotic cell death occurs by inhibition of AKT signaling and activation of the intrinsic apoptotic/caspase pathways. These results raise the possibility that greensporone A could be developed as a therapeutic agent for the treatment of leukemia and other hematological malignancies.

scholarly journals Greensporone C, a Freshwater Fungal Secondary Metabolite Induces Mitochondrial-Mediated Apoptotic Cell Death in Leukemic Cell Lines

2018 ◽  
Vol 9 ◽  
Author(s):  
Kirti S. Prabhu ◽  
Kodappully Sivaraman Siveen ◽  
Shilpa Kuttikrishnan ◽  
Ahmad N. Iskandarani ◽  
Abdul Q. Khan ◽  
...  
Keyword(s):  
Cell Death ◽  
Secondary Metabolite ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Leukemic Cell ◽  
Apoptotic Cell Death ◽  
Leukemic Cell Lines ◽  
Fungal Secondary Metabolite

scholarly journals Induction of Cell Death and Modulation of Annexin A1 by Phytoestrogens in Human Leukemic Cell Lines

2020 ◽  
Author(s):  
Affidah Sabran ◽  
Endang Kumolosasi ◽  
Ibrahim Jantan ◽  
Jamia Azdina Jamal ◽  
Norazrina Azmi ◽  
...  
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Leukemic Cell ◽  
Annexin A1 ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines

Increased Cytotoxicity of 2?,2?-Difluoro-2?-deoxycytidine in Human Leukemic Cell-Lines After a Preincubation with Cyclopentenyl Cytosine

ChemInform ◽  
2005 ◽  
Vol 36 (12) ◽  
Author(s):  
A. C. Verschuur ◽  
A. H. Van Gennip ◽  
R. Leen ◽  
A. B. P. Van Kuilenburg
Keyword(s):  
Cell Lines ◽  
Leukemic Cell ◽  
Human Leukemic Cell ◽  
Leukemic Cell Lines ◽  
Cyclopentenyl Cytosine

scholarly journals Inhibition of Replication Induces Non-Apoptotic Cell Death in Fibroblast Cell Lines Derived from LEC Rats

2003 ◽  
Vol 65 (2) ◽  
pp. 249-254 ◽  
Author(s):  
Masanobu HAYASHI ◽  
Taku HAMASU ◽  
Daiji ENDOH ◽  
Reiko SHIMOJIMA ◽  
Toyo OKUI
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Apoptotic Cell ◽  
Fibroblast Cell ◽  
Apoptotic Cell Death ◽  
Lec Rats ◽  
Fibroblast Cell Lines

scholarly journals ADP-Ribosylation of Actin by the Clostridium botulinum C2 Toxin in Mammalian Cells Results in Delayed Caspase-Dependent Apoptotic Cell Death

2008 ◽  
Vol 76 (10) ◽  
pp. 4600-4608 ◽  
Author(s):  
Karin Heine ◽  
Sascha Pust ◽  
Stefanie Enzenmüller ◽  
Holger Barth
Keyword(s):  
Cell Death ◽  
Cell Lines ◽  
Mammalian Cells ◽  
Clostridium Botulinum ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Adp Ribosylation ◽  
Mammalian Cell Lines ◽  
Adp Ribosyltransferase ◽  
C2 Toxin

ABSTRACT The binary C2 toxin from Clostridium botulinum mono-ADP-ribosylates G-actin in the cytosol of eukaryotic cells. This modification leads to depolymerization of actin filaments accompanied by cell rounding within 3 h of incubation but does not immediately induce cell death. Here we investigated the long-term responses of mammalian cell lines (HeLa and Vero) following C2 toxin treatment. Cells stayed round even though the toxin was removed from the medium after its internalization into the cells. No unmodified actin reappeared in the C2 toxin-treated cells within 48 h. Despite actin being completely ADP-ribosylated after about 7 h, no obvious decrease in the overall amount of actin was observed for at least 48 h. Therefore, ADP-ribosylation was not a signal for an accelerated degradation of actin in the tested cell lines. C2 toxin treatment resulted in delayed apoptotic cell death that became detectable about 15 to 24 h after toxin application in a portion of the cells. Poly(ADP)-ribosyltransferase 1 (PARP-1) was cleaved in C2 toxin-treated cells, an indication of caspase 3 activation and a hallmark of apoptosis. Furthermore, specific caspase inhibitors prevented C2 toxin-induced apoptosis, implying that caspases 8 and 9 were activated in C2 toxin-treated cells. C2I, the ADP-ribosyltransferase component of the C2 toxin, remained active in the cytosol for at least 48 h, and no extensive degradation of C2I was observed. From our data, we conclude that the long-lived nature of C2I in the host cell cytosol was essential for the nonreversible cytotoxic effect of C2 toxin, resulting in delayed apoptosis of the tested mammalian cells.

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