• Title/Summary/Keyword: human leukemia

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Inhibition Effects of Lamellarin D on Human Leukemia K562 Cell Proliferation and Underlying Mechanisms

  • Zhang, Nan;Wang, Dong;Zhu, Yu;Wang, Jian;Lin, Hong
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.22
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    • pp.9915-9919
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    • 2014
  • Lamellarin D (LamD) is a marine alkaloid with a pronounced cytotoxicity against a large panel of cancer cells, affecting cell growth and inducing apoptosis. However, the molecular mechanisms of action of this compound are poorly understood. In this study, the anticancer efficacy of LamD was investigated in human leukemia K562 cells. The results showed suppressed cell proliferation and induction of G0/G1-phase arrest,while expression of CDK1, and activity of smad3 and smad5 were reduced, but that of p27, p53 and STGC3 was increased. LamD induced cell apoptosis through activation of caspases-8/-3, inhibition of survivin and Bcl-2, suggesting that this compound may also act through a caspase-independent pathway. Moreover, LamD inhibited the secretion of TGF-${\beta}$, IL-$1{\beta}$, IL-6, IL-8 and other inflammatory cytokines and the transcriptional activity of transcription factor NF-${\kappa}B$ in human leukemia K562 cells.Taken together, our results suggest that LamD-mediated inhibition of leukemia cell proliferation may be related to the induction of apoptosis and the regulation of cell cycle, tumor-related gene expression and cytokine expression, which may provide a new way of thinking for the treatment leukemia.

Anticancer Effects of Leek Kimchi on Human Cancer Cells

  • Jung, Keun-Ok;Park, Kun-Young;Lloyd B. Bullerman
    • Preventive Nutrition and Food Science
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    • v.7 no.3
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    • pp.250-254
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    • 2002
  • The anticancer effects of leek (buchu in Korean) kimchi were evaluated in the human cancer cells: AGS gastric adenocarcinoma cells, HT-29 human colon adenocarcinoma cells and HL-60 leukemia cells. The leek kimchi (fermented for 6 days at 15$^{\circ}C$) was fractionated into 7 groups: methanol extract, hexane extract, methanol soluble extract MSE), dichloromethane (DCM) fraction (fr.), ethyl acetate fr., butanol fr. and aqueous fr. Most of the leek kimchi tractions inhibited the growth of AGS and HT-29 cancer cells in a dose dependent manner. In particular, the DCM fr. showed the highest inhibitory effect among the tractions. Treatment with the DCM fr. (0.1 mg/mL) reduced the survival rates of AGS and HT-29 cancer cells to 19% and 37% of the controls, respectively. Moreover the DCM fr. of the leek kimchi arrested G2/M phase in the cell cycle and induced apoptosis in HL-60 human promyelocytic leukemia cells. These results indicate that the leek kimchi exerted an anticancer effect on those human cancer cells, and that the DCM fr. arrested G2/M phase in the cell cycle and induced apoptosis in the leukemia cells.

Effects of Rubus Coreanus Miquel on the Apoptosis of U937 Cells (복분자가 U937세포의 apoptosis에 미치는 효과)

  • Lee, Kwang-Kyu;Han, Jong-Hyun;Oh, Chan-Ho
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.6
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    • pp.1404-1408
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    • 2009
  • Methanol extracts of Rubus Coreanus Miquel (RCM) were found to exhibit apoptosis induction of U937 human histiocytic leukemia cells. Treatment of RCM exerted strong cytotoxicity against U937 human leukemia cells. RCM induced apoptosis of U937 leukemia cells in a dose dependent manner. Nitric oxide (NO) production was increased in RCM-treated RAW264.7 macrophage cell line. RCM increased the p53 and $NF{\kappa}B$ gene and decreased the $I{\kappa}B$ gene expression in U937 cells. RCM also increased the $NF{\kappa}B$ protein expression, but decreased the PCNA and BcL-xL protein expression in cultured U937 cells. These data suggest that RCM are effective on the apoptosis induction of human leukemia cells and anti-cancer properties.

Identification of Differentially Expressed Proteins in Imatinib Mesylate-resistant Chronic Myelogenous Cells

  • Park, Jung-Eun;Kim, Sang-Mi;Oh, Jong-K.;Kim, Jin-Y.;Yoon, Sung-Soo;Lee, Dong-Soon;Kim, Young-Soo
    • BMB Reports
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    • v.38 no.6
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    • pp.725-738
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    • 2005
  • Resistance to imatinib mesylate (also known as Gleevec, Glivec, and STI571) often becomes a barrier to the treatment of chronic myelogenous leukemia (CML). In order to identify markers of the action of imatinib mesylate, we used a mass spectrometry approach to compare protein expression profiles in human leukemia cells (K562) and in imatinib mesylate-resistant human leukemia cells (K562-R) in the presence and absence of imatinib mesylate. We identified 118 differentially regulated proteins in these two leukemia cell-lines, with and without a $1\;{\mu}M$ imatinib mesylate challenge. Nine proteins of unknown function were discovered. This is the first comprehensive report regarding differential protein expression in imatinib mesylate-treated CML cells.

CopA3 peptide from Copris tripartitus induces apoptosis in human leukemia cells via a caspase-independent pathway

  • Kang, Bo-Ram;Kim, Ho;Nam, Sung-Hee;Yun, Eun-Young;Kim, Seong-Ryul;Ahn, Mi-Young;Chang, Jong-Soo;Hwang, Jae-Sam
    • BMB Reports
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    • v.45 no.2
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    • pp.85-90
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    • 2012
  • Our previous study demonstrated that CopA3, a disulfide dimer of the coprisin peptide analogue (LLCIALRKK), has antibacterial activity. In this study, we assessed whether CopA3 caused cellular toxicity in various mammalian cell lines. CopA3 selectively caused a marked decrease in cell viability in Jurkat T, U937, and AML-2 cells (human leukemia cells), but was not cytotoxic to Caki or Hela cells. Fragmentation of DNA, a marker of apoptosis, was also confirmed in the leukemia cell lines, but not in the other cells. CopA3-induced apoptosis in leukemia cells was mediated by apoptosis inducing factor (AIF), indicating induction of a caspase-independent signaling pathway.

Monitoring the Expression Profiles of Doxorubicin-Resistant Acute Myelocytic Leukemia Cells by DNA Microarray Analysis

  • Song, Ju-Han;Kim, Tae-Sung
    • Proceedings of the PSK Conference
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    • 2003.10b
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    • pp.167.2-168
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    • 2003
  • Anticancer drug resistance occasionally occurs in malignant hematologic diseases such as acute myelocytic leukemia (AML) treated with chemotherapy and is a major problem to complete remission. Malignant cells primarily induce intrinsic resistance to treatment of anticancer drug, but gradually obtain acquired resistance to cytotoxic activities of chemotherapy. In this study, we monitored the expression profiles of doxorubicin resistance-related genes in AML-2/DX100, a doxorubicin-resistant human acute myelocytic leukemia cell line. (omitted)

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The Effect of Willow Leaf Extracts on Human Leukemic Cells in Vitro

  • El-Shemy, Hany A.;Aboul-Enein, Ahmed M.;Aboul-Enein, Mostafa I.;Issa, Sohair I.;Fujita, Kounosuke
    • BMB Reports
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    • v.36 no.4
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    • pp.387-389
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    • 2003
  • The young developing leaves of willow (Salix safsaf, Salicaceae) trees have antileukemic activity. After a 24-h incubation in vitro, the crude water extracts of the leaves killed a majority of the blasts of acute myeloid leukemia (AML, 73.8%).

23-hydroxyursolic acid Induces Apoptosis of human leukemia HL-60 cells

  • Heon, Won-Jong;Shin, kyung-Min;Rim, Seo-Bo;Park, Hee-Jun;Park, Jong-Won;Lee, Kyung-Tae
    • Proceedings of the PSK Conference
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    • 2002.10a
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    • pp.318.1-318.1
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    • 2002
  • We found that 23-hydroxyursolic acid, triterpenoid was isolated from Cussonia bancoensis have a significant cytotoxic activity against HL -60 human promyelocytic leukemia cells. The IC of 23-hydroxyursolic acid was 32.83 $\mu$M. These anti-proliferative activity was due to induction of apoptosis. The effect of apoptosis was identified by DNA laddering, DAPI assay. PI staining, and Annerxin V-FITC binding assay. (omitted)

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HMGB1 regulates autophagy through increasing transcriptional activities of JNK and ERK in human myeloid leukemia cells

  • Zhao, Mingyi;Yang, Minghua;Yang, Liangchun;Yu, Yan;Xie, Min;Zhu, Shan;Kang, Rui;Tang, Daolin;Jiang, Zhigang;Yuan, Wuzhou;Wu, Xiushan;Cao, Lizhi
    • BMB Reports
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    • v.44 no.9
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    • pp.601-606
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    • 2011
  • HMGB1 is associated with human cancers and is an activator of autophagy which mediates chemotherapy resistance. We here show that the mRNA levels of HMGB1 are high in leukemia cells and it is involved in the progression of childhood chronic myeloid leukemia (CML). HMGB1 decreases the sensitivity of human myeloid leukemia cells K562 to anti-cancer drug induced death through up-regulating the autophagy pathway, which is confirmed by the observation with an increase in fusion of autophagosomes and autophagolysosomes. When overexpressing HMGB1, both mRNA levels of Beclin-1, VSP34 and UVRAG which are key genes involved in mammalian autophagy and protein levels of p-Bcl-2 and LC3-II are increased. Luciferase assays document that over-expression of HMGB1 increases the transcriptional activity of JNK and ERK, which may be silenced by siRNA. The results suggest that HMGB1 regulates JNK and ERK required for autophagy, which provides a potential drug target for therapeutic interventions in childhood CML.

Immunological Studies on the Surface Antigens of Tumor Cells (종양세포 표면항원에 대한 분자면역학적 연구)

  • 김한도;김규원
    • The Korean Journal of Zoology
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    • v.32 no.2
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    • pp.142-152
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    • 1989
  • We have produced a new monoclonal antibody detecting common acute lymphoblastic leukemia antigen (CALLA) and designated as KP-22. CALIA detected by KP-22 is expressed on the all of the various cefl lines examined including common ALL. Burkitt's lymphoma, human fibroblasts and cultured normal human fibroblasts. However out of cell lines tested, a fraction of J-ALL and all of myelocytic leukemia and all other nonleukemia cell lines except for fibroblast are CALIA negative. Immunoprecipitation of solubilized 125 I-labeled membrane proteins from cultured human fibroblasts and leukemia cell lines with KP-22 revealed a major polypeptide chain with an apparent molecular weight of approximately 100 Kd and 95 Kd, respectively. Even though a microheterogeneity in terms of molecular weight between two CALLAs, the peptide mapping patterns of them &e identical indicating that such a microheterogeneity seems to be partly due to heterogeneous terminal sialic acid compositions added by a posttranslational modification process.

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