scholarly journals Diverse autophagy and apoptosis in myeloid leukemia cells induced by 20(s)-GRh2 and blue LED irradiation

RSC Advances ◽  
2019 ◽  
Vol 9 (67) ◽  
pp. 39124-39132
Author(s):  
Jianjian Zhuang ◽  
Juxin Yin ◽  
Chaojian Xu ◽  
Mengmeng Jiang ◽  
Shaowu Lv
Keyword(s):  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Blue Led ◽  
Induced Apoptosis ◽  
Led Irradiation ◽  
In Cells

Blue LED and 20(S)-GRh2 induced apoptosis and autophagy in cells.

scholarly journals Cyclic AMP can promote APL progression and protect myeloid leukemia cells against anthracycline-induced apoptosis

2013 ◽  
Vol 4 (2) ◽  
pp. e516-e516 ◽  
Author(s):  
G Gausdal ◽  
A Wergeland ◽  
J Skavland ◽  
E Nguyen ◽  
F Pendino ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Induced Apoptosis

The inhibition of NF-kB activation decreases the resistance of acute myeloid leukemia cells to TRAIL-induced apoptosis in multicellular aggregates

BIOPHYSICS ◽  
2015 ◽  
Vol 60 (6) ◽  
pp. 953-956 ◽  
Author(s):  
R. S. Fadeev ◽  
M. E. Solovieva ◽  
D. A. Slyadovskiy ◽  
S. G. Zakharov ◽  
I. S. Fadeeva ◽  
...  
Keyword(s):  
Acute Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Multicellular Aggregates ◽  
Acute Myeloid Leukemia Cells ◽  
Induced Apoptosis ◽  
Acute Myeloid

scholarly journals Cleavage of Bcl-2 is an early event in chemotherapy-induced apoptosis of human myeloid leukemia cells

Leukemia ◽  
1999 ◽  
Vol 13 (5) ◽  
pp. 719-728 ◽  
Author(s):  
B Fadeel ◽  
Z Hassan ◽  
E Hellström-Lindberg ◽  
J-I Henter ◽  
S Orrenius ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Early Event ◽  
Induced Apoptosis

Bcr-Abl-Mediated Suppression of Normal Hematopoiesis in Chronic Myeloid Leukemia: Involvement of a Modified Form of NGAL.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2869-2869
Author(s):  
Hui Lin ◽  
Xiaohong Leng ◽  
Tong Sun ◽  
Giuseppe Monaco ◽  
Clifton Stephens ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Hematopoietic Cells ◽  
K562 Cells ◽  
Soft Agar ◽  
Leukemia Cells ◽  
Active Process ◽  
Culture Studies ◽  
Induced Apoptosis

Abstract The BCR-ABL oncogene plays an essential role in chronic myeloid leukemia (CML). In NOD/scid mice injected with soft agar clones of a human CML cell line (K562), we observed a leukemia syndrome involving not only leukemia but also a severe reduction of normal mouse hematopoiesis (Lin et al., Oncogene, 2001). Some of these mice died of a wasting syndrome that involved suppression of hematopoiesis without extensive tumor cell invasion of the spleen and marrow. In CML patients, since normal hematopoietic cells in marrow and spleen are replaced with proliferating leukemic blasts, we postulate that this is an active process mediated by the leukemia cells. The lipocalin 24p3 is secreted by mouse hematopoietic cells deprived of IL-3, resulting in apoptosis induction in a variety of hematopoietic cells including bone marrow cells (Devireddy et al., Science, 2001). We found that BCR-ABL+ mouse hematopoietic cells induce a persistent secretion of a modified form of 24p3 (21 kDa). Co-culture studies show that BCR-ABL+ cells induced apoptosis in BCR-ABL negative cells. Importantly, BCR-ABL+ hematopoietic cells are resistant to apoptosis under the same conditions. Conditioned medium (CM) from BCR-ABL+ cells expressing anti-sense/siRNA 24p3 or CM mixed with 24p3 antibody have reduced apoptotic activity for target cells. We also found that the expression of the Bcr-Abl oncoprotein and its tyrosine kinase are required for induction of 24p3 expression. Leukemic mice induced by BCR-ABL+ cells expressing anti-sense/siRNA 24p3 have increased levels of normal hematopoiesis (marrow and spleen erythropoiesis and blood platelet levels) and reduced invasion of leukemia cells in marrow and spleen tissues, but the leukemia cells readily invade liver and the abdomen as ascites (Lin et al, Oncogene, 2005). These findings indicate that suppression of normal hematopoiesis in BCR-ABL induced leukemia is an active process involving the apoptotic factor 24p3, raising the possibility that similar factors are involved in BCR-ABL+ CML patients. We have found that the K562 clones (Lin et al. 2001) have enhanced expression of NGAL (neutrophil gelatinase-associated lipocalin, human homologue of 24p3) transcripts compared to uncloned K562 cells. We generated additional soft agar K562 clones, each with different expression levels of NGAL transcripts. NOD/scid mice injected with the clone (C5) of K562 cell line expressing a high level of NGAL had severe depression of hematopoiesis and significantly shorter survival time as compared with mice injected with parental K562 cells and a clone (C6) expressing a low level of NGAL. Co-culture studies showed that the C5 K562 clone also induced apoptosis in BCR-ABL negative cells. We detected two glycosylated forms of NGAL/24p3 migrating at 24 kDa and 21 kDa on SDS-PAGE. The 21 kDa form is the major form in CM from mouse BCR-ABL+ cells and K562 clones. Our preliminary data with CML patient samples showed that levels of 21 kDa NGAL protein in bone marrow fluid correlated with BCR-ABL/ABL ratio. Further studies with more patient samples are ongoing to confirm the role of NGAL in suppressing normal hematopoiesis in CML patients and to determine the structural change(s) that leads to the modified form of 24p3/NGAL secreted by CML cells.

Arsenic induces apoptosis of multidrug-resistant human myeloid leukemia cells that express Bcr-Abl or overexpress MDR, MRP, Bcl-2, or Bcl-xL

Blood ◽  
2000 ◽  
Vol 95 (3) ◽  
pp. 1014-1022 ◽  
Author(s):  
Charles Perkins ◽  
Caryn N. Kim ◽  
Guofu Fang ◽  
Kapil N. Bhalla
Keyword(s):  
Myeloid Leukemia ◽  
Blast Crisis ◽  
K562 Cells ◽  
Cell Types ◽  
Multidrug Resistant ◽  
Leukemia Cells ◽  
Protein Levels ◽  
Growth Inhibitory ◽  
Induced Apoptosis

We investigated the in vitro growth inhibitory and apoptotic effects of clinically achievable concentrations of As2O3 (0.5 to 2.0 μmol/L) against human myeloid leukemia cells known to be resistant to a number of apoptotic stimuli. These included chronic myelocytic leukemia (CML) blast crisis K562 and HL-60/Bcr-Abl cells, which contain p210 and p185 Bcr-Abl, respectively, and HL-60 cell types that overexpress Bcl-2 (HL-60/Bcl-2), Bcl-xL(HL-60/Bcl-xL), MDR (HL-60/VCR), or MRP (HL-60/AR) protein. The growth-inhibitory IC50 values for As2O3 treatment for 7 days against all these cell types ranged from 0.8 to 1.5 μmol/L. Exposure to 2 μmol/L As2O3 for 7 days induced apoptosis of all cell types, including HL-60/Bcr-Abl and K562 cells. This was associated with the cytosolic accumulation of cyt c and preapoptotic mitochondrial events, such as the loss of inner membrane potential (▵Ψm) and the increase in reactive oxygen species (ROS). Treatment with As2O3 (2 μmol/L) generated the activities of caspases, which produced the cleavage of the BH3 domain containing proapoptotic Bid protein and poly (ADP-ribose) polymerase. Significantly, As2O3-induced apoptosis of HL-60/Bcr-Abl and K562 cells was associated with a decline in Bcr-Abl protein levels, without any significant alterations in the levels of Bcl-xL, Bax, Apaf-1, Fas, and FasL. Although As2O3 treatment caused a marked increase in the expression of the myeloid differentiation marker CD11b, it did not affect Hb levels in HL-60/Bcr-Abl, K562, or HL-60/neo cells. However, in these cells, As2O3 potently induced hyper-acetylation of the histones H3 and H4. These findings characterize As2O3 as a growth inhibiting and apoptosis-inducing agent against a variety of myeloid leukemia cells resistant to multiple apoptotic stimuli.

scholarly journals STAT pathway in the regulation of zoledronic acid-induced apoptosis in chronic myeloid leukemia cells

2013 ◽  
Vol 67 (6) ◽  
pp. 527-532 ◽  
Author(s):  
Hatice Demet Kiper ◽  
Burcin Tezcanli Kaymaz ◽  
Aysun Adan Gokbulut ◽  
Nur Selvi ◽  
Cigir Biray Avci ◽  
...  
Keyword(s):  
Zoledronic Acid ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Leukemia Cells ◽  
Induced Apoptosis ◽  
Stat Pathway

The histone methyltransferase inhibitor, DZNep, up-regulates TXNIP, increases ROS production, and targets leukemia cells in AML

Blood ◽  
2011 ◽  
Vol 118 (10) ◽  
pp. 2830-2839 ◽  
Author(s):  
Jianbiao Zhou ◽  
Chonglei Bi ◽  
Lip-Lee Cheong ◽  
Sylvia Mahara ◽  
Shaw-Cheng Liu ◽  
...  
Keyword(s):  
Myeloid Leukemia ◽  
Molecular Mechanisms ◽  
Histone Methyltransferase ◽  
Leukemia Cells ◽  
Oxygen Species ◽  
Leukemia Stem Cell ◽  
Polycomb Repressive Complex 2 ◽  
Ros Accumulation ◽  
Direct Target ◽  
Induced Apoptosis

Abstract Recent studies have shown that 3-Deazaneplanocin A (DZNep), a histone methyltransferase inhibitor, disrupts polycomb-repressive complex 2 (PRC2), and preferentially induces apoptosis in cancer cells, including acute myeloid leukemia (AML). However, the underlying molecular mechanisms are not well understood. The present study demonstrates that DZNep induces robust apoptosis in AML cell lines, primary cells, and targets CD34+CD38− leukemia stem cell (LSC)–enriched subpopulations. Using RNA interference (RNAi), gene expression profiling, and ChIP, we identified that TXNIP, a major redox control molecule, plays a crucial role in DZNep-induced apoptosis. We show that disruption of PRC2, either by DZNep treatment or EZH2 knockdown, reactivates TXNIP, inhibits thioredoxin activity, and increases reactive oxygen species (ROS), leading to apoptosis. Furthermore, we show that TXNIP is down-regulated in AML and is a direct target of PRC2-mediated gene silencing. Consistent with the ROS accumulation on DZNep treatment, we also see a signature of endoplasmic reticulum (ER) stress-regulated genes, commonly associated with cell survival, down-regulated by DZNep. Taken together, we uncover a novel molecular mechanism of DZNep-mediated apoptosis and propose that EZH2 may be a potential new target for epigenetic treatment in AML.

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