• Title, Summary, Keyword: HL-60 cells

Search Result 333, Processing Time 0.052 seconds

MISTLETOE (Viscum album var. coloratum) Growing on Carpinus laxiflora BL. Induces the Differentiation of Human Acute Promyeocytic Leukemia (HL-60) Cells

  • Kim, Sang-Cheol;Park, Soo-Young;Hyoun, Jae-Hee;Cho, Hee-Yeong;Lee, Young-Jae;Kang, Ji-Hoon;Lee, Young-Ki;Park, Doek-Bae;Yoo, Eun-Sook;Kang, Hee-Kyoung
    • Toxicological Research
    • /
    • v.20 no.4
    • /
    • pp.307-313
    • /
    • 2004
  • The present study was undertaken to investigate the effects of mistletoe (Viscum album var. coloratum) growing on Carpinus laxiflora BL. on proliferation and differentiation of HL-60 acute promyelocytic leukemia cells. Aqueous extract and its $(NH_2)_2SO_4$ saturated fractions of the mistletoe exhibited potent anti-proliferation activity against HL-60 cells. Moreover, when HL-60 cells were treated with 0~30% and 30~70% $(NH_2)_2SO_4$ saturated fractions of the mistletoe, HL-60 expressed CD 66b or CD 14 cell surface antigens and showed activity to reduce nitroblue tetrazolium, indicating that mistletoe induces the differentiation of HL-60 into granulocytes or monocytes. To understand how mistletoe induces the differentiation, we investigated the expression of molecules for modulating the proliferation and differentiation of leukemia cells, such as c-Myc and myeloblastin. The 0~30% $(NH_2)_2SO_4$ saturated fraction of the mistletoe reduced the mRNA levels of c-Myc and myeloblastin in a time-dependent manner. The results indicate that the mistletoe induces the differentiation of HL-60 cells via the decrease of c-Myc and myeloblastin expressions. Thus, it is suggested that mistletoe has a therapeutic potential for the treatment of acute promyelocytic leukemia.

The Effect of Rice Bran Extract on the Apoptosis Induction of HL-60 Leukemia Cells (미강(Rice Bran) 추출물의 HL-60 백혈병 세포 Apoptosis 유도 효과)

  • Kim, Eun-Ji;Moon, Jungsun;Kang, Jung-Il;Lee, Young-Ki;Koh, Young-Sang;Yoo, Eun-Sook;Kang, Hee-Kyoung;Yim, Dongsool
    • Korean Journal of Pharmacognosy
    • /
    • v.44 no.3
    • /
    • pp.269-274
    • /
    • 2013
  • In this study, we investigated the anticancer effect of rice bran extract in HL-60 human promyelocytic leukemia cells. The extract of rice bran inhibited the proliferation of HL-60 cells. When treated with the rice bran extract, we could observe the apoptotic characteristics such as apoptotic bodies and the increase of sub-G1 hypodiploid cell population, increase of Bax level, decrease of Bcl-2 expression, cleavage of procaspase-3, cleavage of procaspase-9 and cleavage of poly(ADP-ribose) polymerase(PARP) in HL-60 cells. Furthermore, the apoptosis induction of HL-60 cells treated with the rice bran extract was also accompanied by the inactivation of mitogen-activated protein kinases (MAPK) such as ERK1/2 MAPK and p38 MAPK. In addition, the rice bran extract induced the down-regulation of c-myc. These data suggested that the rice bran extract could induce the apoptosis via the inactivation of ERK1/2 MAPK and p38 MAPK, and the down-regulation of c-myc in HL-60 acute pomyelocytic leukemia cells. The results support that the rice bran extract might have potential for the treatment of acute promyelocytic leukemia.

PBK/TOPK Expression During TPA-Induced HL-60 Leukemic Cell Differentiation

  • Liu, Yu-Hong;Gao, Xue-Mei;Ge, Fan-Mei;Wang, Zhe;Wang, Wen-Qing;Li, Xiao-Yong
    • Asian Pacific Journal of Cancer Prevention
    • /
    • v.13 no.5
    • /
    • pp.2145-2148
    • /
    • 2012
  • Objective: This study concerns expression of PBK/TOPK during differentiation of HL-60 leukemic cells induced by tetradecanoyl phorbol acetate (TPA). Methods: Wright-Giemsa staining was performed to observe morphological changes in the HL-60 cells, and flow cytometry was used to assess the cell cycle and CD11b, CD14, CD13, and CD33 expression. PBK/TOPK levels were determined by Western blot analysis. Results: After treating HL60 cells with $5.1{\times}10^{-9}$ mmol/L of TPA for three days, the number of nitroblue-tetrazolium-positive cells and CD11b, CD13, and CD14 expression increased, whereas the PBK/TOPK levels decreased. Conclusions: TPA can inhibit proliferation and induce differentiation of HL60 cells of the granulocytic or monocytic lineage. PBK/TOPK expression was downregulated during this process, whereas the Pho-PBK/TOPK expression was increased.

Effect of 2-Chloromethyl-1-Dihydroxyphosphinylpyrrolidine(2C-1DPP) on Differentiation Induction of Human Leukemia HL-60 Cells (2-Chloromethyl-1-Dihydroxyphosphinylpyrrolidine (2C-1DPP)에 의한 백혈병 세포주 HL-60의 분화유도 효과)

  • Kim, Youg-Mi;Ju, Seong-Min;Park, Jun-Ho;Oh, Jung-Mi;Lee, Chae-Ho;Kim, Eun-Cheol;Jeon, Byung-Hun;Kim, Won-Sin;Kim, Won-Sin
    • Journal of Physiology & Pathology in Korean Medicine
    • /
    • v.21 no.4
    • /
    • pp.940-945
    • /
    • 2007
  • We have examined the induction of HL-60 cell differentiation by treatment of 2-chloromethyl-1-dihydroxyphosphinyl pyrrolidine(2C-1DPP), which is derivative of piperidine and pyrrolidine by ${\alpha}-phosphoramidoakylation$ reaction. It was observed that HL-60 cell proliferation was dose- and time-dependently inhibited by treatment with 2C-1DPP. 2C-1DPP treatment caused a significant change in NBT reduction and enhanced ATRA-induced NBT reduction. Treatment of 2C-1DPP to HL-60 cells increased only CD11b expression in the cells, and also increased markedly G0/G1 stage arrest of HL-60 cells. These results can suggest that 2C-1DPP induced the differentiation of HL-60 cells to granulocytes lineage and enhanced ATRA-induced differentiation. Moreover, DNA expression levels of p27 were up-regulated during 2C-1DPP-dependent HL-60 cell differentiation. Our results suggest that 2C-1DPP have potential as a therapeutic agent in human leukemia.

Expression of ${\alpha}_1$-Acid Glycoprotein and Inflammatory Cytokines during Differentiation of HL-60 Cells

  • Lee, Il-Ha;Kim, In-Sook;Lee, Soo-Young
    • BMB Reports
    • /
    • v.33 no.5
    • /
    • pp.402-406
    • /
    • 2000
  • In order to understand the role of AGP on the differentiation of promyelocytic leukemia cells, the AGP expression and its relation to cytokines were investigated during granulocytic or monocytic differentiation of HL-60 cells. When HL-60 cells were treated with all-trans-retinoic acid (ATRA) for 5 days, the cells were fully differentiated into granulocytes, and the AGP mRNA and protein levels were continuously increased up to 5 days in a dose- and time- dependent manner. However, in the case of the monocytic differentiation of HL-60 cells by tetradeanoyl phorbol acetate (TPA), the AGP gene expression was not induced. In addition, $IL-1{\alpha}$, $IL-1{\beta}$, IL-6 and $TNF-{\alpha}$ mRNAs were also enhanced during granulocytic differentiation. These cytokine transcripts showed a peak level 3 days after the ATRA treatment. It decreased gradually thereafter. However, direct addition of recombinant cytokines ($IL-1{\beta}$, IL-6 and $TNF-{\alpha}$) and dexamethasone to the HL-60 cell cultures showed no AGP induction. These findings suggest that the AGP and proinflammatory cytokines are expressed in ATRA-treated promyelocytic cells. However, these cytokines do not act as autocrine inducers on AGP expression. This fact implies that the AGP expression during granulocytic differentiation of HL-60 cells is induced through a signal pathway different from hepatocyte signaling in inflammation.

  • PDF

Cell Death of Human Promyelocytic Leukemia Cell after Low Dose of Electron Beam Irradiation with TNF-α (저 농도의 전자선을 조사한 전골수구성 백혈병 세포 죽음에서의 TNF-α 작용 효과)

  • Kim, Dong Hyun;Ko, Seong-Jin
    • The Journal of the Korea Contents Association
    • /
    • v.14 no.6
    • /
    • pp.241-246
    • /
    • 2014
  • Acute promyelocytic leukemia (APL) is a cancer of the blood. Although electron beam (EB) irradiation is used with other anti-cancer agents, EB irradiation can be harmful to normal tissues around the cancer. In the present study, we evaluate the differential cytotoxic effect of EB irradiation with other molecules, including TNF-${\alpha}$, on DMSO-treated HL-60 cells and HL-60 cells. HL-60 cells are the human promyleocytic leukemia cell line and are differentiated by DMSO. DMSO-treated HL-60 cells are considered to be normal granulocytic cells. In these results, TNF-${\alpha}$ may be used as the potential agent for the treatment of blood cancer without side effects in low dose of EB irradiation therapy.

Study on Synergistic Anti-tumor Effect of Combination with Adriamycin and Palginhonhapwhajucwhan (팔진탕합화적환(八珍湯合化積丸)과 Adriamycin의 병용처리시 나타나는 synergistic 항종양(抗腫瘍) 효과(效果)에 관(關)한 작용기전 연구(硏究))

  • Moon, Gu;Moon, Seok-Jae;Won, Jin-Hee;Cho, Jung-Yun;Park, Sang-Gu;Song, Bong-Gil;Park, Rae-Gil;Lee, Byung-Gu
    • The Journal of Internal Korean Medicine
    • /
    • v.21 no.3
    • /
    • pp.443-452
    • /
    • 2000
  • Objective : This study was designed to evaluate the synergistic effect on cytotoxicity of combination with adriamycin and Palginhonhapwhajucwhan, a traditional prescription for cancer treatment in oriental medicine, in Chang, HL-60, Hep-3B and Alexander cells. Methods : We observed cell viability in Chang, HL-60, Hep-3B, and Alexander cells by crystal violet staining. Those cells were treated with various concentrations of adriamycin alone, Palginhonhapwhajucwhan alone and combination of two medications for 10 hr. On condition of $0.5{\mu}l/ml$ adriamycin alone, $15.6{\mu}l/ml$ Paljintanghapwhajucwhan alone and combination of two medications, at first, we observed colony forming of Chang and HL-60 cells. Second, we observed DNA fragmentation by agarose electrophoresis in Chang, HL-60, Hep-38 and Alexander cells. Third, we measured the catalytic activation of caspase-1, 2, 3, 6, 8, and 9 protease in Chang cells and caspase-3 protease in Chang, HL-60, Hep-3B and Alexander cells by using fluorogenic substrate. Finally, we isolated mRNA of Fas in Chang, HL-60, Hep-38 and Alexander cells and observed that Fas gene was amplified by RT-PCR Results : 1. The combination of adriamycin and Palginhonhapwhajucwhan synergistically augmented the cytotoxicity of Chang and HL-60 cells whereas did not in Hep-38 and Alexander cells. 2. Cotreatment of two drugs also markedly inhibited the colony forming ability both in Chang and HL-60 cells. 3. The cytotoxicity of these medicatons was revealed as apoptosis characterized by high molecular wight DNA fragmentaton. 4. The apoptotic cytotoxicity was mediated by activation of caspase-3 protease in Chang cells. 5. Synergistic increase in apoptotic cytotoxicity by combination of two medications was dependent on the expression of Fas in cancer cells. Conclusions : Combination of adriamycin and Palginhonhapwhajucwhan significantly augmented apoptotic cytotoxicity of Fas-positive cells such as Chang and HL-60 cells via acticaton of apoptosis signaling pathway.

  • PDF

The Water Extract of Boswellia carterii Induces Apoptosis in Human Leukemia HL-60 Cells (유향 물 추출물의 HL-60 혈액암세포에서 세포사멸 유도효과)

  • 박래길;오광록;이광규;문연자;김정훈
    • YAKHAK HOEJI
    • /
    • v.45 no.2
    • /
    • pp.161-168
    • /
    • 2001
  • The possible mechanism of the antiproliferative and apoptotic effects of Boswellia carterri water extract were studied in HL-60 human leukemia cells. The cytotoxicity of HL-60 cells after the treatment of Boswellia carterii water extract showed dose- and time-dependent manner. The apoptotic effect of 300 $\mu$g/ml Boswellia carterii water extract was demonstrated by DNA laddering. The activity of caspase 3-1ike protease was markedly increased in HL-60 cells treated with Boswellia carterii water extract. Furthermore, the level of Bcl-2 was time-dependently reduced, whereas Bax protein level was enhanced by Boswellia carterii water extract treatment. In conclusion, our results suggest that apoptotic effect of Boswellia carterii water extract may partly mediated through activations of caspase-3 activity and Bax expression, and inhibition of Bcl-2 expression.

  • PDF

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
    • /
    • v.25 no.4
    • /
    • pp.480-484
    • /
    • 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.

Induction of Apoptosis by (-)-epigallocatechin-3-gallate in HL-60 Cells (인체 혈액암세포주(HL-60)에서 (-)-epigallocatechin-3-gallate에 의한 Aapoptosis 유도)

  • 이해미;김연정;박태선
    • Journal of Nutrition and Health
    • /
    • v.36 no.4
    • /
    • pp.382-388
    • /
    • 2003
  • (-)-Epigallocatechin-3-gallate (EGCG) is a polyphenolic compound found in peen tea leaves, and has been known to be one of the most potent catechin species which inhibits cell growth most possibly through an apoptotic cell death. We investigated the apoptotic activity of (-)-EGCG on the human myeloid leukemia cell line, HL-60. Our results of MTT test indicated that (-)-EGCG had a significant antiproliferation effect in HL-60 cells with $IC_{50}$/ (50% inhibition concentration) value of 65 $\mu$M. Giemsa statining of HL-60 cells treated with (-)-EGCG (100 $\mu$M) for 6hrs showed a typical apoptosis-specific morphological change including shrinkage of the cytoplasm, membrane blobbing and compaction of the nuclear chromatin. The DNA fragmentation was observed from the agarose gel electrophoresis of cells treated with (-)-EGCG for 3hrs or longer, and was progressed to a greater degree as treatment time increases. Treatment of the cells with (-)-EGCG (100 $\mu$M) resulted in a rapid release of mitochondrial cytochrome c into the cytosol, and a subsequent cleavage of caspase-3 to an active form in a treatment-time dependent manner. (-)-EGCG (100 $\mu$M) also stimulated proteolytic cleavage of poly-(ADP-ribose) polymerase (PARP) to an active form in HL-60 cells. Tlken together, (-)-EGCG appears to induce the apoptosis in human myeloid leukemia cells via a caspase-dependent pathway. These results suggest the possible application of (-)-EGCG, the major active compound in green tea, as an antiproliferative agent for cancer prevention.