Mitomycin Induced Apoptosis in Human Leukemia K562 Cells

Objective: The research aimed to study the effects of mitomycin on human leukemic K562 cells, and to explore the mechanism of mitomycin induced apoptosis．In order to provide previous experiment basis for mitomycin applying clinical treatments Methods: The multiplication and apoptosis status of K562 cells treated different time by different concentration mitomycin were observed by light microscope, fluorescence microscope, TEM, agrose gel electrophoresis of DNA and flow cytometry. Results: The results showed that mitomycin could induce K562 cells apoptosis, and the best concentration was 12.5μg/ml for 48 h. The optimal concentration of apoptosis induced by apoptosis rate is （28.8±1.04）% （P<0.01）. Mitomycin could affect the S phase among cellular multiplication, cell could be blocked by mitomycin and then apoptosis in this phase. Conclusions: Mitomycin can induce the apoptosis of human leukemic K562 cells. It is of great significance to guide clinical medication.

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Low-dose radiation-induced apoptosis in human leukemia K562 cells through mitochondrial pathways

Molecular Medicine Reports ◽

10.3892/mmr.2014.2381 ◽

2014 ◽

Vol 10 (3) ◽

pp. 1569-1575 ◽

Cited By ~ 3

Author(s):

YONG XIN ◽

HAI-BIN ZHANG ◽

TIAN-YOU TANG ◽

GUI-HONG LIU ◽

JIAN-SHE WANG ◽

...

Keyword(s):

Low Dose ◽

K562 Cells ◽

Human Leukemia ◽

Low Dose Radiation ◽

Radiation Induced ◽

Induced Apoptosis ◽

Dose Radiation ◽

Human Leukemia K562 Cells

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Berbamine-Induced Apoptosis in Human Leukemia K562 Cells.

Blood ◽

10.1182/blood.v104.11.4234.4234 ◽

2004 ◽

Vol 104 (11) ◽

pp. 4234-4234

Author(s):

Xiaoying Zhao ◽

Lei Xu ◽

Dong Wu ◽

Rongzhen Xu

Keyword(s):

Flow Cytometry ◽

Cell Proliferation ◽

Caspase 3 ◽

K562 Cells ◽

Human Leukemia ◽

Dependent Manner ◽

Flow Cytometry Assay ◽

Transcript Levels ◽

Induced Apoptosis ◽

Dose Dependent

Abstract Purpose: To investigate apoptosis-inducing effects of Berbamine on human leukemia cells and to explore the underlying mechanism. Materials and methods: Berbamine was dissolved in 0.9% sodium chloride to an initial concentration of 1mg/ml and subsequently diluted to desired concentrations with cell culture medium. MTT was used to examine the effect of Berbamine on cell proliferation of K562 cells. Characteristic cellular morphological changes were used as indicators of apoptosis in K562 cells while the rate of apoptosis was measured by flow cytometry assay. Expression levels of apoptosis related genes bcl-2 and bax were determined by RT-PCR and the levels of bcr/abl were evaluated by nested-PCR. Levels of Caspase 3 were measured by flow cytometry assay. Results: Berbamine inhibited the cell proliferation significantly and in a dose-dependent manner in tested K562 cells. Its IC50 value was 5.23ug/ml. As determined by morphological observations and flow cytometry assay, Berbamine was able to induce apoptosis of K562 cells within 6 hours. The apoptosis rate of K562 was also dose-dependent. Steady-state transcript levels of bcr/abl decreased dramatically (half-quantity ratio from 1.284 to 0.506 within 72 hours following 8mg/ml Berbamine treatment. On the other hand, the protein levels of Caspase 3 surged from 18.36% to 38.25% (p<0.001) within 24 hours after treatment of 12mg/ml Berbamine. During the same period, no changes of bcl-2 or bax transcript levels were detected in the cells that were treated with 8mg/ml Berbamine. Conclusions: Our results suggest that Berbamine is a potent inhibitor of cell proliferation and a strong inducer of apoptosis in human K562 cells. The Berbamine-induced apoptosis pathway involves down regulation of bcr/abl and up regulation of Caspase 3 expressions. Neither bcl-2 nor bax plays substantial roles in Berbamine-induced K562 cell apoptosis.

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Involvement of p38 MAPK- and JNK-modulated expression of Bcl-2 and Bax in Naja nigricollis CMS-9-induced apoptosis of human leukemia K562 cells

Toxicon ◽

10.1016/j.toxicon.2010.01.024 ◽

2010 ◽

Vol 55 (7) ◽

pp. 1306-1316 ◽

Cited By ~ 35

Author(s):

Ying-Jung Chen ◽

Wen-Hsin Liu ◽

Pei-Hsiu Kao ◽

Jeh-Jeng Wang ◽

Long-Sen Chang

Keyword(s):

P38 Mapk ◽

K562 Cells ◽

Human Leukemia ◽

Induced Apoptosis ◽

Human Leukemia K562 Cells

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Albendazole-Induced SIRT3 Upregulation Protects Human Leukemia K562 Cells from the Cytotoxicity of MCL1 Suppression

International Journal of Molecular Sciences ◽

10.3390/ijms21113907 ◽

2020 ◽

Vol 21 (11) ◽

pp. 3907 ◽

Cited By ~ 1

Author(s):

Liang-Jun Wang ◽

Li-Ren Liou ◽

Yi-Jun Shi ◽

Jing-Ting Chiou ◽

Yuan-Chin Lee ◽

...

Keyword(s):

Ectopic Expression ◽

K562 Cells ◽

Human Leukemia ◽

Cancer Therapies ◽

Microtubule Targeting Agents ◽

Induced Apoptosis ◽

Benzimidazole Anthelmintic ◽

Sirt3 Expression ◽

Human Leukemia K562 Cells

Previous studies have shown that MCL1 stabilization confers cancer cells resistance to microtubule targeting agents (MTAs) and functionally extends the lifespan of MTA-triggered mitotically arrested cells. Albendazole (ABZ), a benzimidazole anthelmintic, shows microtubule-destabilizing activity and has been repositioned for cancer therapies. To clarify the role of MCL1 in ABZ-induced apoptosis, we investigated the cytotoxicity of ABZ on human leukemia K562 cells. Treatment with ABZ for 24 h did not appreciably induce apoptosis or mitochondrial depolarization in K562 cells, though it caused the mitotic arrest of K562 cells. ABZ-evoked p38 MAPK activation concurrently suppressed Sp1-mediated MCL1 expression and increased SIRT3 mRNA stability and protein expression. ABZ and A-1210477 (an MCL1 inhibitor) enhanced the cytotoxicity of ABT-263 (a BCL2/BCL2L1 inhibitor) to their effect on MCL1 suppression. Unlike ABZ, A-1210477 did not affect SIRT3 expression and reduced the survival of K562 cells. Overexpression of SIRT3 attenuated the A-1210477 cytotoxicity on K562 cells. ABZ treatment elicited marked apoptosis and ΔΨm loss in ABT-263-resistant K562 (K562/R) cells, but did not alter SIRT3 expression. Ectopic expression of SIRT3 alleviated the cytotoxicity of ABZ on K562/R cells. Collectively, our data demonstrate that ABZ-induced SIRT3 upregulation delays the apoptosis-inducing effect of MCL1 suppression on apoptosis induction in K562 cells.

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EFFECT OF 12-O-TETRADECANOYLPHORBOL-13-ACETATE ON EXPRESSION OF CELL SURFACE ANTIGENS IN TWO SUBCLONES OF HUMAN LEUKEMIA K562 CELLS

Biological and Pharmaceutical Bulletin ◽

10.1248/bpb.16.1054 ◽

1993 ◽

Vol 16 (10) ◽

pp. 1054-1056

Author(s):

Dai SASAKI ◽

Satoshi KOSUNAGO ◽

Takeshi MIKAMI ◽

Tatsuji MATSUMOTO ◽

Masuko SUZUKI

Keyword(s):

Cell Surface ◽

K562 Cells ◽

Surface Antigens ◽

Human Leukemia ◽

Cell Surface Antigens ◽

Human Leukemia K562 Cells

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Loss of mitochondrial transmembrane potential and glutathione depletion are not sufficient to account for induction of apoptosis by carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone in human leukemia K562 cells

Chemico-Biological Interactions ◽

10.1016/j.cbi.2015.06.033 ◽

2015 ◽

Vol 239 ◽

pp. 100-110 ◽

Cited By ~ 10

Author(s):

Petr Mlejnek ◽

Petr Dolezel

Keyword(s):

Transmembrane Potential ◽

K562 Cells ◽

Mitochondrial Transmembrane Potential ◽

Glutathione Depletion ◽

Human Leukemia ◽

Carbonyl Cyanide ◽

Induction Of Apoptosis ◽

Human Leukemia K562 Cells

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CGP57148B (STI-571) induces differentiation and apoptosis and sensitizes Bcr-Abl–positive human leukemia cells to apoptosis due to antileukemic drugs

Blood ◽

10.1182/blood.v96.6.2246 ◽

2000 ◽

Vol 96 (6) ◽

pp. 2246-2253 ◽

Cited By ~ 192

Author(s):

Guofu Fang ◽

Caryn Naekyung Kim ◽

Charles L. Perkins ◽

Nimmanapalli Ramadevi ◽

Elliott Winton ◽

...

Keyword(s):

Myeloid Leukemia ◽

Fas Ligand ◽

Ectopic Expression ◽

K562 Cells ◽

Parp Cleavage ◽

Human Leukemia ◽

Sti 571 ◽

Tnf Α ◽

Cyt C ◽

Induced Apoptosis

Abstract The differentiation and apoptosis-sensitizing effects of the Bcr-Abl–specific tyrosine kinase inhibitor CGP57148B, also known as STI-571, were determined in human Bcr-Abl–positive HL-60/Bcr-Abl and K562 cells. First, the results demonstrate that the ectopic expression of the p185 Bcr-Abl fusion protein induced hemoglobin in the acute myeloid leukemia (AML) HL-60 cells. Exposure to low-dose cytosine arabinoside (Ara-C; 10 nmol/L) increased hemoglobin levels in HL-60/Bcr-Abl and in the chronic myeloid leukemia (CML) blast crisis K562 cells, which express the p210 Bcr-Abl protein. As compared with HL-60/neo, HL-60/Bcr-Abl and K562 cells were resistant to apoptosis induced by Ara-C, doxorubicin, or tumor necrosis factor-α (TNF-α), which was associated with reduced processing of caspase-8 and Bid protein and decreased cytosolic accumulation of cytochrome c (cyt c). Exposure to CGP57148B alone increased hemoglobin levels and CD11b expression and induced apoptosis of HL-60/Bcr-Abl and K562 cells. CGP57148B treatment down-regulated antiapoptotic XIAP, cIAP1, and Bcl-xL, without affecting Bcl-2, Bax, Apaf-1, Fas (CD95), Fas ligand, Abl, and Bcr-Abl levels. CGP57148B also inhibited constitutively active Akt kinase and NFκB in Bcr-Abl–positive cells. Attenuation of NFκB activity by ectopic expression of transdominant repressor of IκB sensitized HL-60/Bcr-Abl and K562 cells to TNF-α but not to apoptosis induced by Ara-C or doxorubicin. Importantly, cotreatment with CGP57148B significantly increased Ara-C– or doxorubicin-induced apoptosis of HL-60/Bcr-Abl and K562 cells. This was associated with greater cytosolic accumulation of cyt c and PARP cleavage activity of caspase-3. These in vitro data indicate that combinations of CGP57148B and antileukemic drugs such as Ara-C may have improved in vivo efficacy against Bcr-Abl–positive acute leukemia.

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