• Title/Summary/Keyword: HL-60 Cells

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Acteoside induce antiproliferation and differentiation on HL-60, Human leukemia cell line, by cell cycle arrest.

  • Lee, Kyoung-Won;Choi, Jung-Hye;Lee, Kyung-Tae;Lee, Yong-Sup;Kim, Hyoung-Ja;Park, Hee-Juhn
    • Proceedings of the PSK Conference
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    • 2003.04a
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    • pp.215.1-215.1
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    • 2003
  • We investigated the in vitro effect of Acteoside , phenylpropanoid glycosides. is a natural product isolated from …. on proliferation, differentiation and cell cycle regulation in human promyelocytic HL -60 leukemia cells. Acteoside significantly inhibited the proliferation of HL -60 cells, with IC50 of about 30$\mu\textrm{g}$/$m\ell$. It was also found to be a potent inducer of differentiation in human leukemia derived HL-60 cells through the examination of differentiation markers. (omitted)

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Extracellular ATP Induces Apoptotic Signaling in Human Monocyte Leukemic Cells, HL-60 and F-36P

  • Yoon, Mi-Jung;Lee, Hae-Jin;Kim, Jae-Hwan;Kim, Dong-Ku
    • Archives of Pharmacal Research
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    • v.29 no.11
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    • pp.1032-1041
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    • 2006
  • Extracellular adenosine 5'-triphosphate (ATP) affects the function of many tissues and cells. To confirm the biological activity of ATP on human myeloid leukemic cells, F-36P and HL-60, cells were treated with a variety of concentrations of ATP. The stimulation with extracellular ATP induced the arrest of cell proliferation and cell death. from the analysis of Annexin-V staining and caspase activity by flow cytometry. The Annexin-V positive cells in both cell lines were dramatically increased following ATP stimulation. The expression of P2 purinergic receptor genes was confirmed, such as P2X1, P2X4, P2X5, P2X7 and P2Y1, P2Y2, P2Y4, P2Y5, P2Y6, P2Y11 in both leukemic cell lines. Interestingly, ATP induced intracellular calcium flux in HL-60 cells but not in F-36P cells, as determined by Fluo-3 AM staining. Cell cycle analysis revealed that ATP treatment arrested both F-36P and HL-60 cells at G1/G0. Taken together, these data showed that extracellular ATP via P2 receptor genes was involved in the cell proliferation and survival in human myeloid leukemic cells, HL-60 and F-36P cells by the induction of apoptosis and control of cell cycle. Our data suggest that treatment with extracellular nucleotides may be a novel and powerful therapeutic avenue for myeloid leukemic disease.

Comparative susceptibility of different cell lines for culture of Toxoplasma gondii in vitro (톡소플라스마 곤디의 세포내 배양에 있어서 세포 주에 따른 감수성 비교)

  • 박병규;문형로
    • Parasites, Hosts and Diseases
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    • v.31 no.3
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    • pp.215-222
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    • 1993
  • In order to establish a useful cell culture system for T gondii we compared the degree of proliferation of T gondii tachyzoites among 8 different cell lines: 2 kinds of normal animal cells (MDCK-canine kidney cells; Vero-monkey kidney cells) and 6 kinds of human tumor cells (A 549, PC 14-lung cancer cells; SNU 1, SNU 16. Mlm 45-stomach cancer cells; HL-60-promyelocytic leukemia cells), through morphological observation and 3H-uracil uptake assay. The degree of susceptibility to infection with T gondii tachyzoites was highest in A 549 and PC 14 cells, medium in Vero, HL-60, MDCK and SNU 1, and lowest in SNU 16 and MBm 45 cells. The kinetics of T gondii multiplication during the post-Infection 60 hours were higllly dependent upon the dose of tachyzoites administered and the duration among the 8 tested fur the growth and multiplication of T gondii in vitro.

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Codonoposide $1_c$ is a potent inducer of apoptosisin Human Leukemia cell line, HL-60.

  • Lee, Kyung-Won;Lee, Kyung-Tae;Park, Hee-Juhn;Choi, Jong-Won
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.159.2-159.2
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    • 2003
  • Codonopside lc is an active natural compound isolated from the roots of Codonopsis lanceolata (Campanulaceae), a Korean medicinal herb. In the present study, we investigated the in vitro effect of Codonopside 1c on the proliferation and induction of apoptosis in HL-60 human promyelocytic cells. When HL-60 cells were treated with Codonopside 1c, evidence of apoptotic features, including DNA fragmentation, formation of DNA ladder in agarose gel elecrophoresis and increse of annexin V binding, were obtained. (omitted)

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The Effects of Crinum asiaticum on the Apoptosis Induction and the Reversal of Multidrug Resistance in HL-60/MX2

  • Hyun, Jae-Hee; Kang, Jung-Il;Kim, Sang-Cheol;Kim, Elvira;Kang, Ji-Hoon;Kwon, Jung-Mi;Park, Doek-Bae;Lee, Young-Jae;Yoo, Eun-Sook;Kang, Hee-Kyoung
    • Toxicological Research
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    • v.24 no.1
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    • pp.29-36
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    • 2008
  • The present study investigated the anti-proliferative and chemosensitizing effects of Crinum asiaticum var. japonicum against multi-drug resistant (MDR) cancer cells. The 80% methanol extract, chloroform ($CHCl_3$) fraction and butanol (BuOH) fraction of C. asiaticum inhibited the growth of mitoxantrone (MX) resistant HL-60 (HL-60/MX2) cells. When HL-60/MX2 cells were treated with the $CHCl_3$ and BuOH fractions, DNA ladder and sub-G1 hypodiploid cells were observed. Furthermore, the fractions reduced BcI-2 mRNA levels, whereas Bax mRNA levels were increased. These results suggest that the inhibitory effect of C. asiaticum on the growth of the HL-60/MX2 cells might arise from the induction of apoptosis. Treatment of HL-60/MX2 cells with the fractions markedly decreased the mRNA levels of the multi-drug resistance protein-1 and breast cancer resistance protein. The $CHCl_3$ fraction and hexane fraction increased MX accumulation in HL-60/MX2 cells. These results imply that the $CHCl_3$ fraction of C. asiaticum plays a pivotal role as a chemosensitizer. We suggest that components of C. asiaticum might have a therapeutic potential for the treatment of MDR leukemia.

Apoptosis-inducing Effect of Fructus Trichosanthis in HL-60 Leukemic Cells (백혈병 세포주 HL-60에서 과루실 세포고사 유도 효과)

  • Kwon Kang Beom;Kim Eun Kyung;Han Mi Jeong;Ryu Do Gon
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.19 no.4
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    • pp.903-907
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    • 2005
  • Many naturally occurring plant extracts are studied for their beneficial effects for health and particularly on cancer. Apoptosis, or programmed cell death, occurs in both normal and pathological conditions, including cancer Dysregulation of apoptosis allows transformed cells to continually and uninhibitedly enter the cell cycle, thus perpetuating the sequence of mutation, genomic instability and, finally, oncogenesis. To investigate the apoptosis-inducing effect of the extract of Fructus Trichosanthis (EFT) on leukemic HL-60 cells and its mechanism, HL-60 cells in vitro in culture medium were given different doses of the extract. The inhibitory rate of cells were measured by microculture tetrazolium assay, cell apoptotic rate was detected by flow cytometry, morphology of cell apoptosis was observed by DAPI fluorescence staining, and the activations of caspases and PARP were detected using Western blotting analysis. The extract could activate the caspase-3 and caspase-8, induce PARP cleavage, inhibit growth of HL-60 cells, and cause apoptosis significantly The suppression was in dose-dependent manner. Marked morphological changes of cell apoptosis including condensation of chromatin and nuclear fragmentation were observed clearly by DAPI fluorescence staining especially. These results will provide strong laboratory evidence of EFT for clinical treatment of acute leukemia.

Apoptosis-inducing Effect of Fructus Trichosanthis in HL-60 Leukemic Cells (백혈병 세포주 HL-60에서 과루실(瓜蔞實)의 세포고사 유도 효과)

  • Kwon, Kang-Beom;Kim, Eun-Kyung;Han, Mi-Jeong;Ryu, Do-Gon
    • The Journal of Traditional Korean Medicine
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    • v.15 no.1
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    • pp.83-89
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    • 2006
  • Many naturally occurring plant extracts are studied for their beneficial effects for health and particularly on cancer. Apoptosis, or programmed cell death, occurs in both normal and pathological conditions, including cancer. Dysregulation of apoptosis allows transformed cells to continually and uninhibitedly enter the cell cycle, thus perpetuating the sequence of mutation, genomic instability and, finally, oncogenesis. To investigate the apoptosis-Inducing effect of the extract of Fructus Trichosanthis (EFT) on leukemic HL-60 cells and its mechanism, HL-60 cells in vitro in culture medium were given different doses of the extract. The inhibitory rate of cells were measured by microculture tetrazolium assay, cell apoptotic rate was detected by flow cytometry, morphology of cell apoptosis was observed by DAPI fluorescence staining, and the activations of caspases and PARP were detected using Western blotting analysis. The extract could activate the caspase-3 and caspase-8, induce PARP cleavage, inhibit growth of HL-60 cells, and cause apoptosis significantly. The suppression was in dose-dependent manner. Marked morphological changes of cell apoptosis including condensation of chromatin and nuclear fragmentation were observed clearly by DAPI fluorescence staining especially. These results will provide strong laboratory evidence of EFT for clinical treatment of acute leukemia.

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Anti-tumor effect of new compound, 127, through the induction of apoptosis (새로운 화합물 c-127의 세포고사 유도에 의한 항암효과)

  • Baek, Ki Hwan;Han, A Lum;Shin, Sae Ron;Jin, Chun Mae;Yoon, Young Wook;Yu, Seung Taek;Kim, Jong Duk;Choi, Du Young
    • Clinical and Experimental Pediatrics
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    • v.52 no.6
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    • pp.696-700
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    • 2009
  • Purpose : We screened more than 350 compounds with an endoperoxide ring structure in search of an anti-leukemic drug and found that compound 127 (c-127) could induce significant cytotoxicity in HL-60 cells. In this study, we investigated the molecular mechanisms of compound 127-induced antitumor activity on HL-60 cells. Methods : HL-60 cells were cultured in Rosewell Park Memorial Institute 1640 and cell viability was measured by MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide], a tetrazole assay. Apoptosis was assessed by a DNA fragmentation test. Apoptotic machineries were determined by Western blot analysis. Results : C-127 could induce a cytotoxic effect at 24 h and apoptosis at 6 h, which was demonstrated with MTT assay and DNA fragmentation test, respectively. The apoptotic effect of this drug was caused by the activation of the intracellular caspase-8,3 activation, the cleavage of pro-apoptotic Bid, and the increase of c-Jun expression accompanied with JNK (Jun N-terminal kinases) phosphorylation. On the contrary, it increased the expression of anti-apoptotic Bcl-2 levels, leading to the induction of the induction of anti-apoptotic effect. Taken together, the present study demonstrated that c-127 was a potent inducer of cytotoxicity on HL-60 cells through apoptotic mechanisms, which included the activation of caspase family, the regulation of Bcl-2 family, and the activation of JNK signaling pathway. Conclusion : Our results suggest that c-127 has a strong antitumor activity through the regulation of various apoptotic machineries on HL-60 cells. The compound may be utilized as an effective and potentially therapeutic drug in leukemia.

Studies on Gene Expression of baicalin treated in HL-60 cell line using High-throughput Gene Expression Analysis Techniques (Baicalin을 처리한 HL-60 백혈병 세포주에서 대규모 유전자 분석 발현 연구)

  • Kang Bong Joo;Cha Min Ho;Jeon Byung Hun;Yun Yong Gab;Yoon Yoo Sik
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.18 no.5
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    • pp.1291-1300
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    • 2004
  • Baicalin, a biologically active flavonoid form the roots of Scutallaria baicalensis (Skullcap), have been reported to not only function as anti-oxidants but also cause anticancer effect. We investigated the mechanism of baicalin-induced cytotoxicity and the macro scale gene expression analysis in leukemia cell line, HL-60 cells. Baicalin (10 μM) were used to treat the cells for 6h, 12h, 24h, 48h and 72h. In a human cDNAchip study of 65,000 genes evaluated 6, 12, 24, 48. 72 hours after treated with Baicalin in HL-60 cells. Hierarchical cluster against the genes which showed expression changes by more than two fold. One hundred one genes were grouped into 6 clusters according to their profile of expression by a hierarchical clustering algorithm. For genes differentially expressed in response to baicalin treatment, we tested functional classes based on Gene Ontology (GO) terms. This study provides the most comprehensive available survey of gene expression changes in response to baicalin treatment in HL-60 cell line.

Induction of the apoptosis of HL -60 leukemia cells by Scytosiphon lomentaria

  • Kim, Sang-Chul;Park, Soo-Young;Hyoun, Jae-Hee;Kang, Ji-Hoon;Lee, Young-Ki;Park, Deok-Bae;Yoo, Eun-Sook;Kang, Hee-Kyoung
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 2003.11a
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    • pp.81-81
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    • 2003
  • The present study was taken to examine the inhibitory effect of extracts of Scytosiphon lomentaria, a marine alga growing in Jeju Island, on the growth of cancer cells and to develop an anti-cancer agent using components of S. lomemtaria. The effect was observed by the measurement of metabolic activity using colorimetric 3-(4,5-dimethylthiazol)-2,5-diphenyltetrazolium bromide (MTT) assay. In results, crude extract of this alga markedly inhibited the growth of leukemia cell lines such as HL-60 and KG-1, but could scarcely inhibit the growth of normal cells (HEL299) and adenocarcinoma cells (SNU-16 and HCT-I5). When HL-60 cells were treated with the extract, DNA fragmentation and the increase of proportion of sub-G1 hypodiploid cells were observed. Therefore, the inhibitory effect of S. lomemtaria on the growth of HL-60 cells seems to arise from the induction of apoptosis. In order to understand the mechanism of apoptosis inducton by S. lomemtaria, we examined the changes of Bcl-2 and Bax expression. The extract reduced Bcl-2, an anti-apoptotic protein, but increased Bax, a pro-apoptotic protein in a dose-dependent manner. When we examined the activation of caspase-3, an effector of apoptosis, the expression of active form(19 kDa) of caspase-3 was increased and the increase of their activities was demonstrated by the cleavage of poly(ADP-ribose)polymerase, a substrate of caspase-3, to 85 kDa. The results indicate that extract of S. lomentaria induces the apoptosis of HL-60 cells via the down-regulation of Bc1-2 and the activation of caspases.

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