Induction of G 2 /M phase arrest and apoptosis by the flavonoid tamarixetin on human leukemia cells

2013 ◽  
Vol 53 (12) ◽  
pp. 939-950 ◽  
Author(s):  
Fabio Nicolini ◽  
Olga Burmistrova ◽  
María Teresa Marrero ◽  
Fernando Torres ◽  
Cristina Hernández ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

Betuletol 3-methyl ether induces G2 -M phase arrest and activates the sphingomyelin and MAPK pathways in human leukemia cells

2009 ◽  
Vol 49 (1) ◽  
pp. 32-43 ◽  
Author(s):  
Sara Rubio ◽  
José Quintana ◽  
José L. Eiroa ◽  
Jorge Triana ◽  
Francisco Estévez
Keyword(s):  
Methyl Ether ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Mapk Pathways ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

Induction of G2/M phase arrest and apoptosis of human leukemia cells by potent antitumor triazoloacridinone C-1305

2006 ◽  
Vol 72 (12) ◽  
pp. 1668-1679 ◽  
Author(s):  
Ewa Augustin ◽  
Anna Moś-Rompa ◽  
Anna Skwarska ◽  
Jacek M. Witkowski ◽  
Jerzy Konopa
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

Induction of G2-M phase arrest and apoptosis by α-methylene-γ-butyrolactones in human leukemia cells

2008 ◽  
Vol 269 (1) ◽  
pp. 139-147 ◽  
Author(s):  
Fernando Torres ◽  
José Quintana ◽  
Javier Cabrera ◽  
Juan F. Loro ◽  
Francisco León ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

MZ3 can induce G2/M-phase arrest and apoptosis in human leukemia cells

2008 ◽  
Vol 134 (12) ◽  
pp. 1337-1345 ◽  
Author(s):  
Liang Fang ◽  
Li Shen ◽  
Yanfen Fang ◽  
Yongzhou Hu ◽  
Qiaojun He ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

Thimerosal induces apoptosis and G2/M phase arrest in human leukemia cells

2006 ◽  
Vol 45 (9) ◽  
pp. 657-666 ◽  
Author(s):  
Kyung Jin Woo ◽  
Tae-Jin Lee ◽  
Jae Hoon Bae ◽  
Byeong-Churl Jang ◽  
Dae-Kyu Song ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

scholarly journals 2-Phenyl-4-quinolone (YT-1) induces G2/M phase arrest and an intrinsic apoptotic mechanism in human leukemia cells

2017 ◽  
Author(s):  
Meng‑Wei Lin ◽  
Jai‑Sing Yang ◽  
Chi‑Cheng Lu ◽  
Chingju Lin ◽  
Sheng‑Chu Kuo ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase ◽  
Apoptotic Mechanism

scholarly journals N-benzyl-N-methyldecan-1-amine, a phenylamine derivative isolated from garlic cloves, induces G2/M phase arrest and apoptosis in U937 human leukemia cells

2014 ◽  
Vol 32 (1) ◽  
pp. 373-381 ◽  
Author(s):  
JIN-WOO JEONG ◽  
SEJIN PARK ◽  
CHEOL PARK ◽  
YOUNG-CHAE CHANG ◽  
DONG-OH MOON ◽  
...  
Keyword(s):  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
Phase Arrest ◽  
M Phase

c-Myb Plays a Role InG2/M Cell Cycle Transition by Direct Regulation of Cyclin B1 Expression in Hematopoietic Cells.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 1355-1355 ◽  
Author(s):  
Yuji Nakata ◽  
Susan Shetzline ◽  
Chizuko Sakashita ◽  
Anna Kalota ◽  
Andrzej Ptasznik ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Proliferation ◽  
Hematopoietic Cells ◽  
Cyclin B1 ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Human Leukemia Cells ◽  
M Phase ◽  
Cell Cycle Transition ◽  
Myb Protein

Abstract Myb family transcription factors are found throughout the phyla, and recent studies have demonstrated that Drosophila myb, as well as plant and yeast c-myb-like transcription factors, play an important role in regulating transition though the G1/S and G2/M phases of the cell cycle. Myb’s ability to regulate passage through G2/M is due at least in part to its ability to induce Cyclin B1 expression. A recent study in human T98G ganglioblastoma cells revealed that E2F, together with B-Myb, regulated cyclin B1 expression. Though c-myb was expressed in these cells, it was not found in immunoprecipitated E2F-B-Myb protein complexes and for this reason was felt not to participate in cyclin B1 expression in these cells. Since c-myb plays such a critical role in regulating hematopoietic cell proliferation, and its role in regulating G2/M in blood cells has not previously been explored, we investigated whether c-myb was important is regulating this phase of the cell cycle using K562 and Mo7e cells, as well as PHA stimulated human T lymphocytes. In distinct contrast to findings reported for T98G cells, we now report that in normal and malignant human hematopoietic cells, c-Myb directly upregulates cyclin B1 expression. Several lines of evidence support this claim. First, cyclin B1 expression decreased in Mo7e human leukemia cells in which c-myb had been silenced with siRNA. siRNA targeted to B-myb also decreased cyclin B1 expression, while neither siRNA species decreased cdc2 or cyclin A in these cells. As expected, siRNA targeted against c-myb or B-myb impaired Mo7e cell proliferation. Simultaneous exposure to both siRNA blocked proliferation completely. Second, using an alternative strategy, an inducible dominant negative c-Myb protein also decreased cyclin B1 expression in K562 human leukemia cells. The expected consequence of this, accelerated exit from the M phase, was also observed. Third, we examined c-Myb expression in human T cells by western and Real Time PCR, pre and post PHA stimulation. c-Myb expression began to gradually increase in the G1 phase of cell cycle, continued to increase after S phase, with the maximal protein level being found in G2/M phase, and concordant with cyclin B1 expression. These results indicated a correlation between c-Myb and cyclin B1 expression but did not indicate if c-Myb regulated cyclin B1 expression directly. To address this question, several additional experiments were carried out. A CAT assay showed that overexpressing c-Myb protein could increase activity when driven by a cyclin B1 promoter construct ~5X compared to K562 control cells. Next, examination of the cyclin B1 promoter showed eight potential c-Myb binding sites. Two were canonical [5′-pyrimidine AACG/TG-3′] and located upstream of 6 others which were [5′-AACNG-3′] in type. An in vitro c-Myb binding assay revealed that c-Myb bound the canonical sites. We then performed a Chromatin Immunoprecipitation (ChIP) Assay with anti-c-Myb antibody and specifically enriched cyclin B1 promoter DNA sequences which strongly suggested that c-Myb bound the cyclin B1 promoter in vivo. A control antibody was inactive. Finally, a conditionally active c-Myb restored cyclin B1 mRNA expression in K562 human leukemia cells in presence of cycloheximide within 6 hours. Therefore, in addition to its role in regulating G1/S cell cycle transition, c-Myb also regulates cyclin B1 expression and therefore transition through the G2/M phase in human hematopoietic cells.

scholarly journals Combination of cytostatic chemotherapy with cisplatin and photodynamic therapy with Radachlorin reduced resistance of K562 and Hela cell lines

2021 ◽  
Vol 2086 (1) ◽  
pp. 012125
Author(s):  
V V Klimenko ◽  
S V Shmakov ◽  
N A Knyazev ◽  
N A Verlov ◽  
An A Bogdanov ◽  
...  
Keyword(s):  
Photodynamic Therapy ◽  
Combination Index ◽  
Carcinoma Cells ◽  
Leukemia Cells ◽  
Human Leukemia ◽  
Proliferative Effect ◽  
Human Leukemia Cells ◽  
Hela Cell Lines ◽  
Proliferation Activity ◽  
M Phase

Abstract In this work were study combination effect of photodynamic therapy and cisplatin on the proliferation activity of K562 human leukemia cells and Hela cervical carcinoma cells. A decrease in cell viability and an increase the fraction of apoptotic cells for combination treatment compared with single therapy were observed. It has been shown that the G2/M-phase of cell cycle decreases compared with cisplatin treatment alone, which demonstrates an increase anti-proliferative effect. The combination index of the photodynamic therapy with Radachlorin and cisplatin was calculated and indicates a synergistic effect.

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