Mechanism Study of HL-60 Leukemic Cells Proliferative Inhibition Induced by Chinese Medicinal Herbs Mixture Jieduweikang Pill.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 4512-4512
Author(s):  
Ri Zhang ◽  
Pin Wu ◽  
Zi-ling Zhu ◽  
Jiannong Cen ◽  
De Pei Wu
Keyword(s):  
Colony Formation ◽  
Herbal Remedy ◽  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Dependent Manner ◽  
Dna Ladder ◽  
Antitumor Effects ◽  
Concentration Dependent Manner ◽  
Nbt Reduction

Abstract Background. It’s not surprising that the traditional Chinese herbal remedy is yielding useful drug leads. The mixture composed of thirteen Chinese medicinal plants---jieduweikang(JDWK) pill including Qingdai, Qinghao, Huangchi, Baihuasheshecao, Banzhilian and so on has been shown the clinical antitumor effects in China. We here report the mechanism investigation of JDWK pill cytotoxicity to leukemia cell line HL-60. Methods By using the method of serum pharmacology, the serum containing the JDWK pill was collected from rats. The MTT and tumor colony formation were used to determine the effects of JDWK pill on proliferation of HL-60 cells. NBT reduction, DNA electrophoresis, flow cytometry and RT-PCR were used to analyze the differentiation and apoptosis of HL-60 cells after treating with JDWK pill. Elisa was used to assay the secretion of VEGF from HL-60 cells. Results The liquid growth and colony formation of HL-60 cells were evidently inhibited by the serum containing JDWK pill and the cells were shown characteristic DNA “ladder” on agarose gel electrophoresis and more than 20% apoptotic cells in DNA histogram as well as the downregulation of bcl-2 gene related to apoptosis in a concentration-dependent manner, compared with the control. NBT reduction assay indicated that JDWK pill with low concentration may induce myeloid terminal differentiation of HL-60 cells and the level of VEGF was obviously decresed. Conclusion The JDWK pill can exerts the its anti-proliferative effect on the leukemic HL-60 cells through inducing apoptosis relating to the downregulation of Bcl-2 gene and anti-angiogenic effects with higher concentration and inducing myeloid differentiation with lower concentration.

scholarly journals COL-3-Induced Molecular and Ultrastructural Alterations in K562 Cells

2022 ◽  
Vol 12 (1) ◽  
pp. 42
Author(s):  
Mona Fares ◽  
Sandra Oerther ◽  
Kjell Hultenby ◽  
Danica Gubrianska ◽  
Ying Zhao ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Ultrastructural Changes ◽  
Dependent Manner ◽  
Antitumor Effects ◽  
Concentration Dependent Manner ◽  
Transmission Electron Microscopy Analysis

Tetracycline-3 (4-dedimethylamino sancycline, COL-3) is a non-antibiotic tetracycline derivative. COL-3 exerts potent anti-metalloproteinase activity and its antitumor effects have been reported both in vitro and in vivo. In this study, we investigated the mechanisms of COL-3-induced cytotoxicity in a chronic myeloid leukemia cell line, K562, characterized by the BCR–ABL fusion protein. COL-3 induced K562 cell death in a concentration-dependent manner with an IC50 of 10.8 µg/mL and exhibited features of both apoptosis and necrosis. However, flow cytometry analysis revealed that necrotic cells dominated over the early and late apoptotic cells upon treatment with COL-3. Transmission electron microscopy analysis in combination with Western blotting (WB) analysis revealed early mitochondrial swelling accompanied by the early release of cytochrome c and truncated apoptosis inducing factor (tAIF). In addition, ultrastructural changes were detected in the endoplasmic reticulum (ER). COL-3 affected the levels of glucose-regulated protein-94 (GRP94) and resulted in m-calpain activation. DNA double strand breaks as a signature for DNA damage was also confirmed using an antibody against γH2AX. WB analyses did not demonstrate caspase activation, while Bcl-xL protein remained unaffected. In conclusion, COL-3-induced cell death involves DNA damage as well as mitochondrial and ER perturbation with features of paraptosis and programmed necrosis.

scholarly journals Evaluation of the Effects of Some Brazilian Medicinal Plants on the Production of TNF-αand CCL2 by THP-1 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Grasielle S. Gusman ◽  
Priscilla R. V. Campana ◽  
Luciano C. Castro ◽  
Rachel O. Castilho ◽  
Mauro M. Teixeira ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Radical Scavenging Activity ◽  
Radical Scavenging ◽  
Leukemia Cell ◽  
Leukemia Cell Line ◽  
Dependent Manner ◽  
Scavenging Activity ◽  
Monocytic Leukemia ◽  
Concentration Dependent Manner ◽  
Highly Active

Several plant species are traditionally used in Brazil to treat various inflammatory diseases. Tumor necrosis factor- (TNF-)αand chemokine (C-C motif) ligand 2 (CCL2) are key inflammatory mediators in diseases like rheumatoid arthritis and atherosclerosis, respectively; nevertheless, only a few extracts have been assayed against these targets. We herein report the effect of 19 plant extracts on TNF-αand CCL2 release by lipopolysaccharide- (LPS-) stimulated THP-1 cells, a human monocytic leukemia cell line, along with their radical scavenging activity on DPPH. The extracts ofCaryocar brasiliense,Casearia sylvestris,Coccoloba cereifera, andTerminalia glabrescensinhibited TNF-αproduction in a concentration-dependent manner. Fractionation of these extracts potentiated the anti-TNF-αeffect, which was shown to concentrate in polar fractions, mainly composed by polyphenols. Significant CCL2 inhibition was elicited byLippia sidoidesandTerminalia glabrescensextracts, whose fractionation resulted in highly active low polar fractions. All assayed extracts showed strong radical scavenging activity, but antioxidant activity did not correlate with inhibition of TNF-αor CCL2 production. Our results allowed identifying extracts with selective capacity to block cytokine production; therefore, further purification of these extracts may yield molecules that could be useful in the treatment of chronic inflammatory diseases.

Multiparametric Evaluation of Retinoic Acid-Induced Terminal Differentiation of Blastoid Cells from Acute Non-Lymphocytic Leukemia Patients in Vitro

1989 ◽  
Vol 75 (5) ◽  
pp. 435-442
Author(s):  
Kalpana S. Joshi ◽  
S.G. Ananda Rao ◽  
D.S. Joshi ◽  
S. Nene ◽  
S.H. Advani ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Leukemia Cell ◽  
Lymphocytic Leukemia ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Granulocytic Differentiation ◽  
Dna And Rna ◽  
Dna And Rna Synthesis ◽  
Nbt Reduction

Recent findings that retinoic acid (RA) induces terminal granulocytic differentiation of the human promyelocytic leukemia cell line HL-60 in vitro and blast cell maturation in patients suffering from acute non-lymphocytic leukemia (ANLL) prompted an investigation on the ability of this agent to induce terminal maturation in blast cells from ANLL patients in vitro. We tested the ability of RA at 3×10–6 M, 3×10–7 M and 3×108– M concentrations to induce differentiation in blastold cells from 16 patients with ANLL using cytochemical and cytologic parameters, in addition to cytofluorometric methods. Leukemic cells in primary culture from all the patients underwent cytochemical and biochemical changes after treatment with RA. However, the extent of differentiation-positive cell clones (D+ clones) varied from patient to patient. Morphologic maturation was observed in a significant number of bone marrow samples. Leukocyte alkaline phosphatase and NBT reduction ability of cells, which are biochemical markers of granulocytic differentiation, were also significantly increased with a simultaneous decrease in DNA and RNA synthesis (which was estimated using a Phywe ICP-11 impulse flow cytometer).

scholarly journals Human acute leukemia cell line with the t(4;11) chromosomal rearrangement exhibits B lineage and monocytic characteristics

Blood ◽  
1985 ◽  
Vol 65 (1) ◽  
pp. 21-31 ◽  
Author(s):  
RC Stong ◽  
SJ Korsmeyer ◽  
JL Parkin ◽  
DC Arthur ◽  
JH Kersey
Keyword(s):  
Acute Leukemia ◽  
Cell Line ◽  
Lymphoblastic Leukemia ◽  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Immunoglobulin Gene ◽  
A Cell ◽  
B Lineage

Abstract A cell line, designated RS4;11, was established from the bone marrow of a patient in relapse with an acute leukemia that was characterized by the t(4;11) chromosomal abnormality. The cell line and the patient's fresh leukemic cells both had the t(4;11)(q21;q23) and an isochromosome for the long arm of No. 7. Morphologically, all cells were lymphoid in appearance. Ultrastructurally and cytochemically, approximately 30% of the cells possessed myeloid features. The cells were strongly positive for terminal deoxynucleotidyl transferase. They were HLA-DR positive and expressed surface antigens characteristic for B lineage cells, including those detected by anti-B4, BA-1, BA-2, and PI153/3. Immunoglobulin gene analysis revealed rearrangements of the heavy chain and kappa chain genes. The cells lacked the common acute lymphoblastic leukemia antigen and antigenic markers characteristic of T lineage cells. The cells reacted with the myeloid antibody 1G10 but not with other myeloid monoclonal antibodies. Treatment with 12-O-tetradecanoyl- phorbol-13-acetate induced a monocyte-like phenotype demonstrated by cytochemical, functional, immunologic, and electron microscopic studies. The expression of markers of both early lymphoid and early myeloid cells represents an unusual phenotype and suggests that RS4;11 represents a cell with dual lineage capabilities. To our knowledge, RS4;11 is the first cell line established from t(4;11)-associated acute leukemia.

scholarly journals A monoclonal antibody reacting with human basophils

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1414-1418
Author(s):  
MP Bodger ◽  
GL Mounsey ◽  
J Nelson ◽  
PH Fitzgerald
Keyword(s):  
Monoclonal Antibody ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Hel Cells ◽  
Basophilic Leukemia Cell ◽  
Human Basophils ◽  
Basophilic Leukemia

Bsp-1 is an IgM murine monoclonal antibody raised against the human erythroblastic leukemia cell line (HEL) that reacts with basophils but not neutrophils or eosinophils. Western blotting techniques showed that Bsp-1 reacts with a 45-kilodalton surface antigen on HEL cells. The distribution of Bsp-1 antigen on leukemic cells is confined to a basophilic leukemia cell line, KU812, chronic myeloid leukemia with basophilia, and some cases of acute undifferentiated leukemia. Bsp-1 might therefore be a useful reagent for the study of basophil function and differentiation.

scholarly journals Expression of the Wilms' Tumor Suppressor Gene, WT1, Is Upregulated by Leukemia Inhibitory Factor and Induces Monocytic Differentiation in M1 Leukemic Cells

Blood ◽  
1998 ◽  
Vol 91 (3) ◽  
pp. 764-773 ◽  
Author(s):  
Shirley I. Smith ◽  
Dominique Weil ◽  
Gregory R. Johnson ◽  
Andrew W. Boyd ◽  
Chung L. Li
Keyword(s):  
Leukemia Inhibitory Factor ◽  
Wilms Tumor ◽  
Leukemia Cell ◽  
Inhibitory Factor ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Specific Cell ◽  
Monocytic Differentiation ◽  
Macrophage Differentiation ◽  
Molecular Control

The Wilms' tumor gene, WT1, encodes a transcription factor of the Cys2-His2 zinc finger type. The functional significance of WT1 expression in leukemias, in addition to tissues and cell lines of hematopoietic origin, has not been determined. Using the murine myeloblastic leukemia cell line M1 as a model for macrophage differentiation, expression of WT1 is shown to be activated in M1 cells 24 hours after differentiation induction by leukemia inhibitory factor (LIF). Upregulation ofWT1 in these cells is associated with cellular differentiation, coinciding with expression of the monocyte/macrophage marker c-fms, and the appearance of mature cells. WT1 isoforms lacking the KTS insert are unable to be ectopically expressed in M1 cells. Stable expression of the WT1 isoforms containing the KTS insert leads to spontaneous differentiation of the M1 myeloblasts through the monocytic differentiation pathway. These cells express c-fms,in addition to the myeloid-specific cell surface marker Mac-1. Exposure of these cells to LIF results in the rapid onset of terminal macrophage differentiation, accompanied by apoptotic cell death. These results show that the WT1 gene is an important regulator of M1 cell monocytic differentiation in vitro, and suggests a potential role for this gene in the molecular control of hematopoiesis.

scholarly journals Induction of apoptosis by Kola nut extract as a recent and promising treatment strategy for Leukemia

Bionatura ◽  
2021 ◽  
Vol 6 (2) ◽  
pp. 1725-1732
Author(s):  
Hamdah Alsaeedi ◽  
Rowaid Qahwaji ◽  
Talal Qadah
Keyword(s):  
Cell Cycle ◽  
Cell Line ◽  
Leukemia Cell ◽  
K562 Cells ◽  
Myelogenous Leukemia ◽  
Time Dependent ◽  
Leukemia Cell Line ◽  
Apoptotic Cells ◽  
Dependent Manner ◽  
Anti Cancer

Kola nut extracts have recently been reported to contain chemopreventive compounds providing several pharmacological benefits. This study investigated Kola nut extracts' anti-cancer activity on human immortalized myelogenous leukemia cell line K562 through apoptosis and cell cycle arrest. Fresh Kola nuts were prepared as powder and dissolved in DMSO. Different concentrations (50, 100, 150, 200, and 250 μg/ml) of working solutions were prepared. The K562 cells were treated with the different concentrations of Kola nut extract or vehicle control (10% DMSO) followed by incubation at 37°C for 24, 48, and 72 hours, respectively. Treatment activity was investigated in K562 cells; by Resazurin, and FITC/Propidium Iodide and 7-AAD stained cells to evaluate apoptotic cells and the cell cycle's progression. Inhibition of leukemia cell proliferation was observed. The extract effectively induced cell death, early and late apoptosis by approximately 30% after 24 and 48 hours incubation, and an increase in the rate of dead cells by 50% was observed after 72 hours of incubation. Also, cell growth reduction was seen at high dose concentrations (150 and 200 µg/ml), as evident by cell count once treated with Kola nut extract. The total number of apoptotic cells increased from 5.8% of the control group to 27.4% at 250 µg/ml concentration. Moreover, Kola nut extracts' effects on K562 cells increased gradually in a dose and time-dependent manner. It was observed that Kola nut extracts could arrest the cell cycle in the G2/M phase as an increase in the number of cells by 29.8% and 14.6 % were observed from 9.8% and 5.2% after 24 and 48 hours of incubation, respectively. This increase was detected in a dose and time-dependent manner. Kola nut extracts can be used as a novel anti-cancer agent in Leukemia treatment as it has shown significant therapeutic potential and therefore provides new insights in understanding the mechanisms of its action. Keywords: Kola nut extracts, Leukemia, K562 cell line, Apoptosis, Cancer.

Betulinic acid induces apoptosis of gallbladder cancer cells via repressing SCD1

2020 ◽  
Vol 52 (2) ◽  
pp. 200-206 ◽  
Author(s):  
Hongfei Wang ◽  
Fangxiao Dong ◽  
Ye Wang ◽  
Xu’an Wang ◽  
Defei Hong ◽  
...  
Keyword(s):  
Gallbladder Cancer ◽  
Betulinic Acid ◽  
Polymerase Chain Reaction Analysis ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Antitumor Effects ◽  
Concentration Dependent Manner ◽  
Polymerase Chain ◽  
Induced Apoptosis ◽  
Scd1 Expression

Abstract Gallbladder cancer (GBC) is the most common and aggressive malignancy of the biliary tract. Betulinic acid (BetA) has been reported to have anti-inflammatory and antitumor effects; however, the effect of BetA on GBC is still unknown. In this study, we investigated the effect of BetA on five GBC cell lines and found that BetA significantly inhibited the proliferation of NOZ cells but had little inhibitory effect on other GBC cells. BetA disturbed mitochondrial membrane potential and induced apoptosis in NOZ cells. Real-time polymerase chain reaction analysis revealed that stearoyl-coenzyme A desaturase 1 (SCD1) was highly expressed in NOZ cells but low expressed in other GBC cells. BetA inhibited SCD1 expression in a concentration-dependent manner in NOZ cells. Downregulation of SCD1 expression by RNA interference inhibited the proliferation of NOZ cells and induced cell apoptosis. Moreover, BetA inhibited the growth of xenografted tumors and suppressed SCD1 expression in nude mice. Thus, our results showed that BetA induced apoptosis through repressing SCD1 expression in GBC, suggesting that BetA might be an effective agent for the treatment of patients with GBC that highly expresses SCD1.

scholarly journals A monoclonal antibody reacting with human basophils

Blood ◽  
1987 ◽  
Vol 69 (5) ◽  
pp. 1414-1418 ◽  
Author(s):  
MP Bodger ◽  
GL Mounsey ◽  
J Nelson ◽  
PH Fitzgerald
Keyword(s):  
Monoclonal Antibody ◽  
Cell Line ◽  
Myeloid Leukemia ◽  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Hel Cells ◽  
Basophilic Leukemia Cell ◽  
Human Basophils ◽  
Basophilic Leukemia

Abstract Bsp-1 is an IgM murine monoclonal antibody raised against the human erythroblastic leukemia cell line (HEL) that reacts with basophils but not neutrophils or eosinophils. Western blotting techniques showed that Bsp-1 reacts with a 45-kilodalton surface antigen on HEL cells. The distribution of Bsp-1 antigen on leukemic cells is confined to a basophilic leukemia cell line, KU812, chronic myeloid leukemia with basophilia, and some cases of acute undifferentiated leukemia. Bsp-1 might therefore be a useful reagent for the study of basophil function and differentiation.

scholarly journals Curcumin and Its Analogue Induce Apoptosis in Leukemia Cells and Have Additive Effects with Bortezomib in Cellular and Xenograft Models

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
L. I. Nagy ◽  
L. Z. Fehér ◽  
G. J. Szebeni ◽  
M. Gyuris ◽  
P. Sipos ◽  
...  
Keyword(s):  
Leukemia Cell ◽  
Leukemic Cells ◽  
Leukemia Cell Line ◽  
Leukemia Cells ◽  
Great Promise ◽  
Human Leukemia ◽  
Human Leukemia Cell Line ◽  
Apoptotic Effects

Combination therapy of bortezomib with other chemotherapeutics is an emerging treatment strategy. Since both curcumin and bortezomib inhibit NF-κB, we tested the effects of their combination on leukemia cells. To improve potency, a novel Mannich-type curcumin derivative, C-150, was synthesized. Curcumin and its analogue showed potent antiproliferative and apoptotic effects on the human leukemia cell line, HL60, with different potency but similar additive properties with bortezomib. Additive antiproliferative effects were correlated well with LPS-induced NF-κB inhibition results. Gene expression data on cell cycle and apoptosis related genes, obtained by high-throughput QPCR, showed that curcumin and its analogue act through similar signaling pathways. In correlation with in vitro results similar additive effect could be obsereved in SCID mice inoculated systemically with HL60 cells. C-150 in a liposomal formulation given intravenously in combination with bortezomib was more efficient than either of the drugs alone. As our novel curcumin analogue exerted anticancer effects in leukemic cells at submicromolar concentration in vitro and at 3 mg/kg dose in vivo, which was potentiated by bortezomib, it holds a great promise as a future therapeutic agent in the treatment of leukemia alone or in combination.

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