|
Leukemia, Myelocytic, Acute
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
We investigated the effects and underlying mechanisms of cyanidin-3-o-β-glucoside (Cy-3-g, the major bioactive compound in anthocyanins) on the apoptosis of human primary megakaryocytes and Meg-01 cell line in vitro<i>.</i> We found that Cy-3-g dose-dependently increased the dissipation of the mitochondrial membrane potential, caspase-9 and caspase-3 activity in megakaryocytes from patients with newly diagnosed acute myeloid leukaemia but not in those from healthy volunteers.
|
29864778 |
2018 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Moreover, flow cytometry of AML cells revealed increased apoptosis with 4f (10 μM) treatment for 48 h. The protein levels of cleaved caspase-3 and cleaved poly (ADP-ribose) polymerase were enhanced in all three AML cell types.
|
28032588 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
Biomarker
|
disease |
BEFREE |
Collectively, these data highlight Caspase-3 as an important regulator of autophagy in AML and demonstrate that the balance and selectivity between its substrates can dictate the pace of disease.
|
28381396 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
Biomarker
|
disease |
BEFREE |
Results showed that AHCC induced Caspase-3-dependent apoptosis in AML cell lines as well as in primary AML leukopheresis samples.
|
28727820 |
2017 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
Biomarker
|
disease |
BEFREE |
We show that (a) APcK110 inhibits proliferation of the mastocytosis cell line HMC1.2 and the SCF-responsive cell line OCI/AML3 in a dose-dependent manner; (b) APcK110 is a more potent inhibitor of OCI/AML3 proliferation than the clinically used Kit inhibitors imatinib and dasatinib and at least as potent as cytarabine; (c) APcK110 inhibits the phosphorylation of Kit, Stat3, Stat5, and Akt in a dose-dependent fashion, showing activity of APcK110 on Kit and its downstream signaling pathways; (d) APcK110 induces apoptosis by cleavage of caspase-3 and poly(ADP-ribose) polymerase; and (e) APcK110 inhibits proliferation of primary AML blasts in a clonogenic assay but does not affect proliferation of normal colony-forming cells.
|
19383925 |
2009 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
Biomarker
|
disease |
BEFREE |
VX-680-induced cell death in AML cell lines was accompanied by formation of monopolar mitotic spindles, G(2)/M phase arrest, decreased phosphorylated(p)-Akt-1, and increased proteolytic cleavage of procaspase-3 and poly(ADP)ribose polymerase.
|
18160664 |
2008 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
AlteredExpression
|
disease |
BEFREE |
Smac sensitized human acute myeloid leukaemia blasts to cytochrome c-induced activation of caspase-3.
|
12642862 |
2003 |
|
Leukemia, Myelocytic, Acute
|
0.080 |
Biomarker
|
disease |
BEFREE |
High levels of inactive, uncleaved caspase 2 and caspase 3 have recently been associated with poor survival in patients with acute myelogenous leukemia.
|
10632337 |
1999 |