• 제목/요약/키워드: HL60 cell

검색결과 308건 처리시간 0.025초

Cell Cycle Arrest and Apoptotic Induction by MCS-C2 in Human Leukemia HL-60 Cells

  • Kim, Min-Kyoung;Lee, Chul-Hoon
    • 한국미생물생명공학회:학술대회논문집
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    • 한국미생물생명공학회 2004년도 Annual Meeting BioExibition International Symposium
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    • pp.297-301
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    • 2004
  • The purpose of the present study was to investigate the anti-proliferative and apoptotic effects of MCS-C2, a novel analogue of toyocamycin and sangivamycin, in human promyelocytic leukemia (HL-60) cells. When treated with MCS-C2, inhibited proliferation associated with cell cycle arrest and apoptotic induction was found in the HL-60 cells in a concentration-dependent and time-dependent manner. This apoptotic induction was associated with the cleavage of Bid and a release of cytochrome c from mitochondria into the cytosol, followed by the activation of caspase-3 and inactivation of poly (ADP-ribose) polymerase (PARP). However, there was no significant change in any other mitochondrial membrane proteins, such as Bcl-2 and Bax. Consequently, the current findings suggest that the mitochondrial pathway was primarily involved in the MCS-C2-induced apoptosis in the human promyelocytic leukemia HL-60 cells.

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HL-60 백혈병 세포의 세포고사에 미치는 저근백피의 효과 (Effect of Ailanthi Cortex on the Apoptosis and Cell Cycle of HL-60 Leukemia Cell Line)

  • 정영목;박신기;이준;김영목;윤용갑;김원신;한동민;안원근;윤유식;전병훈
    • 동의생리병리학회지
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    • 제17권4호
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    • pp.914-922
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    • 2003
  • Ailanthus altissima has been used to settle an upset stomach, to alleviate a fever, and as an insecticide. We reported that the water extract of A. altissima induced apoptotic cell death in HL-60 human leukemia cell line. Here, we showed the dose-dependent inhibitions of cell viability by the extract, as measured by cell morphology. The cell cycle control genes are considered to play important roles in tumorigenesis. The purpose of the present study is also to investigate the effect of A. altissima on cell cycle progression and its molecular mechanism in the cells. The level of p21 protein was increased after treatment of the extract, whereas both Bcl-2 and Bax protein levels were not changed. These results suggest that A. altissima induces apoptotic cell death via p21-dependent signaling pathway in HL-60 human leukemia cell line which delete wild type p53. G1 checkpoin related gene products tested (cyclin D3, cyclin dependent kinase 4, retinoblastoma, E2F1) were decreased in their protein levels in a dose-dependent manner after treatment of the extract. Taken together, these results indicate that the increase of apoptotic cell death by A. altissima may be due to the inhibition of cell cycle in HL-60 human leukemia cell line

생약으로부터 세포분화유도물질의 검색 및 분리 및 분리 (I) (Screening and Isolation of the Cell Differentiation Inducers from Medicinal Plants (I))

  • 박은정;김진웅
    • 생약학회지
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    • 제28권4호
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    • pp.225-232
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    • 1997
  • 300 extracts derived from 100 plants were tested for their potential to induce HL-60 cell differentiation using NBT assay and NSE/SE staining methods. Morphological changes from suspended to adherent state of the cells were also observed by microscopic examination. In result, 55 extracts induced cell differentiation into monocyte/macrophage lineage in the NBT and the NSE assay.

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Regulation of Caspase Activity During Apoptosis Induced by Baicalein in HL60 Human Leukemia Cell Line

  • Byun, Boo-Hyeong;Kim, Bu-Yeo
    • Food Science and Biotechnology
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    • 제17권6호
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    • pp.1305-1309
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    • 2008
  • Baicalein, one of the major flavonoid in Scutellaria baicalensis, has been known for its effects on proliferation and apoptosis of many tumor cell lines. Most biological effects of baicalein are thought to be from its antioxidant and prooxidant activities. In this report, baicalein was found to induce apoptosis in HL60 human promyelocytic leukemia cell line. Baicalein treatment induced DNA fragmentation and typical morphological features of apoptosis. To elucidate the mechanism of baicalein-induced apoptosis, the activities of the members of caspase family were measured. Interestingly caspase 2, 3, and 6 were significantly activated whereas caspase 1, 8, and 9 were not activated, suggesting selective involvement of specific caspases. Further, treatment with caspase inhibitors also supports the involvement of caspase 2 in apoptosis process. Although it has been reported that baicalein can induce apoptosis through many caspase pathways, the present study indicates that caspase 2 not caspase 9 pathway may be the important step in apoptosis on HL60 cell line.

왕지네(Scolopendra subspinipes mutilans)의 Bcl-xL 조절에 의한 HL-60 세포의 아폽토시스(Apoptosis) 유도 (Induction of Apoptosis by Scolopendra subspinipes mutilans in Human Leukemia HL-60 Cells through Bcl-xL Regulation)

  • 김길남;김상범;윤원종;양경식;박수영
    • 한국식품영양과학회지
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    • 제37권11호
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    • pp.1408-1414
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    • 2008
  • 왕지네 에탄올 추출물 및 순차적 분획물 중 디클로로메탄과 에틸아세테이트 분획물에서 HL-60 세포 성장이 강하게 억제되었다. 또한, 디클로로메탄과 에틸아세테이트 분획물을 처리하였을 때 apoptosis의 특징인 DNA 절편화, 핵의 응축과 apoptotic body가 관찰되었다. 이는 왕지네 분획물의 암세포성장 억제가 apoptosis에 의해 억제되는 것을 알 수 있었다. 디클로로메탄과 에틸아세테이트 분획물의 apoptosis 유도는 anti-apoptosis 단백질인 Bcl-xL의 억제를 통하여 apoptosis 유도가 시작되고 세포사멸에 직접적으로 영향을 미치는 casapse-3과 PARP의 활성을 일으켜 apoptosis를 유도하였다. 본 연구는 왕지네의 항암효과를 과학적 근거를 제시하고 기능성식품이나 항암제로 개발할 있는 가능성을 제시하였다. 향후 왕지네를 이용한 제품의 개발을 위해서는 유효성분의 동정 및 그 성분의 작용 기전에 대한 추가 연구가 필요할 것으로 보인다.

Mechanism of Apoptotic Cell Death by 2,4,3',5'-Tetramethoxystilbene in Human Promyelocytic Leukemic HL-60 Cells

  • Lee, Sang-Kwang;Chae, Ah-Reum;Chun, Young-Jin
    • Biomolecules & Therapeutics
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    • 제15권3호
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    • pp.145-149
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    • 2007
  • We have previously shown that 2,4,3',5'-tetramethoxystilbene (TMS), a synthetic trans-stilbene analogue acting as a potent inhibitor of human cytochrome P450 1B1, induces apoptotic cell death in human cancer cells. In the present studies, we report the mechanisms of apoptotic cell death by TMS in human promyelocytic leukemic HL-60 cells. We found that treatment of HL-60 cells with TMS suppressed the cell growth in a concentration-dependent manner with $IC_{50}$ value of about 0.8 ${\mu}M$. Immunoblot experiments revealed that DMHS-induced apoptosis was associated with cleavage of poly (ADP-ribose) polymerase. The release of cytochrome c from mitochondria into the cytosol was significantly increased in response to TMS. TMS caused activation of caspase-3 in a concentration-dependent manner and TMS-mediated caspase-3 activation was partially prevented by the caspase inhibitor, zVAD-fmk. Interestingly, we found that the cytotoxic effect of anticancer drugs such as paclitaxel, docetaxel, or etoposide was enhanced in the presence of TMS. Simultaneous treatment with TCDD also significantly increased cytotoxic effects of TMS alone or TMS and anti-cancer agents. Taken together, our present results indicated that TMS leads to apoptotic cell death in HL-60 cells through activation of caspase-3 activity and release of cytochrome c into cytosol. The ability of TMS to increase cytotoxic effect of anticancer drugs may contribute to its usefulness for cancer chemotherapy.

Costunolide Induces Differentiation of Human Leukemia HL-60 Cells

  • Choi, Jung-Hye;Seo, Bo-Rim;Seo, Seong-Hoon;Lee, Kyung-Tae;Park, Jae-Hoon;Park, Hee-Juhn;Choi, Jong-Won;Yoshie-Itoh;Miyamoto, Ken-Ichi
    • Archives of Pharmacal Research
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    • 제25권4호
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    • pp.480-484
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    • 2002
  • Costunolide has been reported to be a cytotoxic and chemopreventive agent. This work investigated the mechanism of the anti proliferative effect of costunolide and determined that it induced differentiation of the human leukemia cell line HL-60. Costunolide exhibited a potent antiproliferative activity against HL-60 cells. It was also found to be a potent inducer of differentiation in human leukemia derived HL-60 cells through the examination of differentiation markers, as assessed by the reduction of nitroblue tetrazolium, the increase in esterase activities and phagocytic activity, morphology change and the expression of CD14 and CD66b surface antigens. These results, accompanied by a decline in the expression of c-myc protein, suggest that costunolide induces differentiation of human leukemia cells to granulocytes and monocytes/macrophages lineage.

HL-60 세포에 대한 Triterpent Acids와 Ginsenosides의 분화효과 (Effects of Triterpence Acids and Ginsenosides in Differentiation of HL-60 Promyelocytic Leckemia Cells)

  • 강창모;이호영;김신일;김규원
    • 생명과학회지
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    • 제8권2호
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    • pp.162-166
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    • 1998
  • 전 골수성 백혈병 세초인 HL-60 세포를 model로 하여, 민간요법으로 사용되어져 부작용이 극히 적은 거승로 알려진 고려인삼의 구성 성분 중 주요성분이 ginseng (Panzx ginseng C.A. Meyer) saponin 및 ginsenoside Rh1, Rh2, Rh3, 비파 (Eriobotrya japonica L.) 잎의 성분들 중에서 항발암 및 항암성분으로 알려진 ursolic acid 및 oleanolic acid, 웅담중의 중요성분 성분인 lithocholoc acid 드잉 분화능력이 있는 지를 조사하고자 본 실험을 수행아였다. Retinoic acid를 처리한 결과 타 연구자들의 연구결과들처럼 높은 분화력을 관찰할 수 있었으며, dbcAMP 단독 처리군에서도 높은 분화효과를 나타냈었다. Dexamethasone 처리군에서는 분화효과를 거의 관찰할 수 없었으나,dexamethansone과 구조적으로 유사한 ursolic acid와 oleanolic acid는 보다 높은 분화력을 보였고 웅담성분의 중요성분인 lirhocholic acid는 높은 분화력을 나타냈었다. Ginseng saponin은 0.00375% (w/v)에서 20% 이상의 분화력을 보였으며, Ginsenoside Rh2와 Rh3는 높은 분화력을 나타냈다.

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문주란 추출물의 HL-60 백혈병 세포 Apoptosis 유도 효과 (Apoptosis Induction of HL-60 Leukemia Cells by Extract of Crinum asiaticum)

  • 현재희;김엘비라;강정일;김상철;유은숙;강희경
    • 약학회지
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    • 제52권1호
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    • pp.1-6
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    • 2008
  • The present study investigated the antiproliferative effects of Crnum asiaticum var. japonicum against HL-60 human leukemia cells. The 80% MeOH extract or several solvent fractions from the C. asiaticum inhibited the growth of HL-60 cells, whereas the growth of HEL-299 cells, human embryonic lung fibroblast, was scarcely inhibited. When the HL-60 cells were treated with the $CHCl_3$ fraction, the BuOH fraction, the EtOAc fraction and the $H_2O$ fraction, DNA ladder, chromatin condensation and increase of sub-G1 hypodiploid cells were observed. Furthermore, the $CHCl_3$ fraction and the BuOH fraction reduced Bc1-2 mRNA level, whereas Bax mRNA level was increased. These results suggest that the inhibitory effect of C. asiaticum on the growth of the HL-60 cell might be mediated through the induction of apoptosis via the down-regulation of Bc1-2. Taken together, components of C. asiaticum might have a therapeutic potential for the treatment of human leukemia.