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At least 19 recordsLinked to original sources
PubMed1992

Patterns of alpha-L-fucosidase in acute myeloid leukemia cells. Comparison with promyelocytic HL-60 cell line.

Changes were observed in alpha-L-fucosidase forms in cells from acute myelocytic leukemias (AML). Total alpha-L-fucosidase activity was not significantly different for normal granulocytes and leukemic cells, but enzymic profiles obtained by chromatofocusing are quite different. In granulocyte profile, two main peaks are present (B and more acidic A) which were eluted at pH 5.2 with a shoulder at pH 4.6. In AMLs the B form is present but weakly expressed, whereas the more acidic forms are the major ones. This pattern may be related either to the malignancy character or to the stage at which the differentiation is stopped. Experiments on an HL-60 cell line (promyelocytic cells corresponding to the AML 3 type) showed that differentiation induced by dimethyl sulfoxide leads to the appearance of the B form present in normal mature cells. Thus the repartition of the enzyme forms seems to be related to the stage of differentiation of the myelocytic cells.

Acute Disease↗
PubMed1979

Normal functional characteristics of cultured human promyelocytic leukemia cells (HL-60) after induction of differentiation by dimethylsulfoxide.

The HL-60 human promyelocytic leukemia cell line can be induced to terminally differentiate to mature myeloid cells sharing a number of functional characteristics with normal granulocytes including response to chemoattractants, development of complement receptors, phagocytosis, superoxide production, and nitroblue tetrazolium dye reduction. Hence the Me2SO-induced HL-60 cells provide a unique in vitro model for studying various important aspects of human myeloid cell differentiation.

Binding Sites↗
PubMed1992

[The effects of retinoic acid and recombinant human granulocyte colony-stimulating factor on alkaline phosphatase activity of HL-60 cells].

We examined alkaline phosphatase (ALP) activity in the HL-60 cell induced by retinoic acid (RA) and recombinant human granulocyte colony-stimulating factor (rhG-CSF). rhG-CSF induced a small but significant increase of NBT-reducing ability and ALP activity of the HL-60 cells. Among various inducers of cell differentiation, 1,25(OH)2D3 and dimethylsulfoxide (DMSO) caused the increase of the NBT-reducing ability and the suppression of ALP activity induced by rhG-CSF, while RA enhanced both of them. Protein kinase C inhibitors (H-7 and staurosporine) but not a protein kinase A inhibitor (HA1004) significantly suppressed the ALP activity induced by the simultaneous treatment with RA and rhG-CSF.

Alkaline Phosphatase↗
PubMed1992

Formyl peptides and ATP stimulate Ca2+ and Na+ inward currents through non-selective cation channels via G-proteins in dibutyryl cyclic AMP-differentiated HL-60 cells. Involvement of Ca2+ and Na+ in the activation of beta-glucuronidase release and superoxide production.

In human neutrophils, the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L-phenylalanine (fMLP) induces increases in the intracellular free Ca2+ concentration ([Ca2+]i) with subsequent activation of beta-glucuronidase release and superoxide (O2-) production. Results from several laboratories suggest that the increase in [Ca2+]i is due to activation of non-selective cation (NSC) channels. We studied the biophysical characteristics, pharmacological modulation and functional role of NSC channels in dibutyryl cyclic AMP (Bt2cAMP)-differentiated HL-60 cells. fMLP increased [Ca2+]i by release of Ca2+ from intracellular stores and influx of Ca2+ from the extracellular space. fMLP also induced Mn2+ influx. Ca2+ and Mn2+ influxes were inhibited by 1-(beta-[3-(4-methoxyphenyl)propoxy]-4-methoxyphenethyl)-1H-imidazole hydrochloride (SK&F 96365). Under whole-cell voltage-clamp conditions, fMLP and ATP (a purinoceptor agonist) activated inward currents characterized by a linear current-voltage relationship and a reversal potential near 0 mV. NSC channels were substantially more permeable to Na+ than to Ca2+. SK&F 96365 inhibited fMLP- and ATP-stimulated currents with a half-maximal effect at about 3 microM. Pertussis toxin prevented stimulation by fMLP of NSC currents and reduced ATP-stimulated currents by about 80%. Intracellular application of the stable GDP analogue, guanosine 5'-O-[2-thio]diphosphate, completely blocked stimulation by agonists of NSC currents. In excised inside-out patches, single channel openings with an amplitude of 0.24 pA were observed in the presence of fMLP and the GTP analogue, guanosine 5'-O-[3-thio]triphosphate. The bath solution contained neither Ca2+ nor ATP. The current/voltage relationship was linear with a conductance of 4-5 pS and reversed at about 0 mV. fMLP-induced beta-glucuronidase release and O2- production were substantially reduced by replacement of extracellular CaCl2 or NaCl by ethylenebis(oxyethylenenitrilo)tetra-acetic acid and choline chloride respectively. In the absence of Ca2+ and Na+, fMLP was ineffective. SK&F 96365 inhibited fMLP-induced beta-glucuronidase release and O2- production in the presence of both Ca2+ and Na+, and in the presence of Ca2+ or Na+ alone. NaCl (25-50 mM) enhanced the basal and absolute extent of fMLP-stimulated GTP hydrolysis of heterotrimeric regulatory G-proteins in HL-60 membranes. The order of effectiveness of salts in enhancing GTP hydrolysis was LiCl > KCl > NaCl > choline chloride.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMedDate not supplied

Puromycin is a potent and specific inhibitor of tyrosine kinase activity in HL-60 cells.

The search for specific tyrosine kinase inhibitors constitutes a novel approach to the development of anticancer agents. Puromycin (PM) inhibits protein synthesis by causing the premature release of truncated PM-peptide complexes (PMPs), the structure of which predicts an inhibitory effect on tyrosine kinase activity (21). The present study was undertaken to investigate the effects of a low dose of PM (0.9 microM) on tyrosine kinase activity in HL-60 leukaemic cells. Experiments were specifically controlled to exclude inhibitory effects consequent on protein synthesis blockade. Soluble enzyme extracts derived from PM-treated cells showed attenuated phosphorylation of two independent synthetic tyrosine kinase-specific substrates, the polymer Poly(Glu:Tyr; 4:1) and the peptide substrate Raytide. In contrast, Protein Kinase C-specific activity was unaffected by PM-exposure. It is possible that inhibition was due to metabolites of PM, perhaps PMPs, rather than to PM itself. Whether the inhibition of tyrosine kinase activity observed with the substrates used in this study is equally applicable to all tyrosine kinases, is not yet clear. Nevertheless, low-dose PM could provide a useful tool for dissecting out the role of tyrosine phosphorylation in the regulation and dysregulation of cell growth, and could conceivably prove beneficial in the treatment of tumours in which tyrosine kinase overactivity is linked to oncogenesis.

Cycloheximide↗
PubMed1992

Bone marrow stromal cells attenuate mitoxantrone cytotoxicity against HL-60 leukemic cells.

We evaluated the effect of cultured human bone marrow (BM) stromal cells on the cytotoxicity of mitoxantrone (MIT) against the HL-60 leukemic cell line. BM-derived fibroblastoid cells (BMFC) suppressed colony formation of HL-60 cells in the absence of MIT. BMFC increased the survival of HL-60 colony-forming cells in the presence of 50 ng/ml MIT. A significant decrease in the drug concentration was not detected on BMFC. Our results suggest that BM stromal cells can modulate the antileukemic effect of an anticancer drug.

Cell Adhesion↗
PubMed1979

Chromatin conformation during cell differentiation of human myeloid leukemia cells.

A novel human promyelocytic leukemia cell line (HL-60) has been shown to form terminally differentiated granulocytes in the presence of dimethyl-sulfoxide (DMSO), some other chemicals, or colony stimulating factor. Compared to chromatin from HL-60 cells, chromatin from DMSO treated HL-60 cells showed an enrichment in low temperature melting material. The decrease in thermostability of chromatin from HL-60 cells after DMSO treatment is similar to the shift in thermostability of chromatin from human lymphocytes after stimulation with phytohemagglutinin (PHA). These results suggest that changes in the thermostability of chromatin may not be specific for cell differentiation or PHA stimulation.

Adult↗
PubMed1979

Functional changes in human leukemic cell line HL-60. A model for myeloid differentiation.

Polar solvents induce terminal differentiation in the human promyelocytic leukemia cell line HL-60. The present studies describe the functional changes that accompany the morphologic progression from promyelocytes to bands and poly-morphonuclear leukocytes (PMN) over 9 d of culture in 1.3 percent dimethylsulfoxide (DMSO). As the HL-60 cells mature, the rate of O(2-) production increase 18-fold, with a progressive shortening of the lag time required for activation. Hexosemonophosphate shunt activity rises concomitantly. Ingestin of paraffin oil droplets opsonized with complement or Ig increases 10-fold over 9 d in DMSO. Latex ingestion per cell by each morphologic type does not change significantly, but total latex ingestion by groups of cells increases with the rise in the proportion of mature cells with greater ingestion capacities. Degranulation, as measured by release of beta-glucuronidase, lysozyme, and peroxidase, reaches maximum after 3-6 d in DMSO, then declines. HL-60 cells contain no detectable lactoferrin, suggesting that their secondary granules are absent or defective. However, they kill staphylococci by day 6 in DMSO. Morphologically immature cells (days 1-3 in DMSO) are capable of O(2-) generation, hexosemonophosphate shunt activity, ingestion, degranulation, and bacterial killing. Maximal performance of each function by cells incubated in DMSO for longer periods of time is 50-100 percent that of normal PMN. DMSO- induced differentiation of HL-60 cells is a promising model for myeloid development.

Cell Differentiation↗
PubMed1979

Characterization of the continuous, differentiating myeloid cell line (HL-60) from a patient with acute promyelocytic leukemia.

In a prelminary communication, we described the establishment of a continuous human myeloid cell line (HL-60). Here we report the detailed properties of this cell line and document its derivation from the peripheral blood leukocytes of a patient with acute promyelocytic leukemia. As characterized by light and electron microscopy, the predominant cell type in both the fresh and cultured sources is a neutrophilic promyelocyte with prominent nuclear/cytoplasmic asynchrony. Up to 10% of the cultured cells spontaneously differentiate beyond the promyelocyte stage, and the proportion of terminally differentiated cells is markedly enhanced by compounds known to stimulate differentiation of mouse (Friend) erythroleukemia cells. The HL-60 cells lack specific markers for lymphoid cells, but express surface receptors for Fc fragment and complement (C3), which have been associated with differentiated granulocytes. They exhibit phagocytic activity and responsiveness to a chemotactic stimulus commensurate with the proportion of mature cells. As characteristic of transformed cells, the HL-60 cells form colonies in semisolid medium and produce subcutaneous myeloid tumors (chloromas) in nude mice. A source of colony-stimulating activity stimulated the cloning efficiency in soft agar 5--30-fold. Despite adaptations to culture, the morphological phenotype and responsiveness to chemical induction of differentiation is essentially unchanged through at least 85 passages. Cytogenetic studies reveal aneuploidy. Metaphases with 44 chromosomes predominated in vivo and in early culture passages; however, clones with 45 or 46 chromosomes became predominant with continued passaging. The most consistent karyotypic abnormalities were the deletion of chromosomes 5, 8, and X and the addition of a marker resembling a D-group acrocentric and of a submetacentric marker, most likely an abnormal E-group chromosome. No DNA herpesvirus or RNA retrovirus was isolated in the fresh or cultured cells. The HL-60 cultured cell line provides a continuous source of human cells for studying the molecular events of myeloid differentiation and the effects of physiologic, pharmacologic, and virologic elements on this process.

Adult↗
PubMed1992

Inhibitors of proteases prevent endonucleolysis accompanying apoptotic death of HL-60 leukemic cells and normal thymocytes.

Exposure of human promyelocytic leukemic HL-60 cells to the topoisomerase I inhibitor camptothecin (CAM) triggers endonucleolytic activity and apoptotic death of these cells. The nucleolytic effect is seen 2-4 h after drug addition and is highly selective to cells progressing through S phase. Concomitant with degradation of DNA, which is preferential to the nucleosomal DNA linker sections, extensive proteolysis takes place in these cells. Cellular RNA, however, is initially degraded to a much lesser degree than DNA or protein. Both endonucleolysis and proteolysis triggered by CAM in S-phase HL-60 cells can be prevented by the protease inhibitors N-tosyl-L-phenylalanylchloromethyl ketone (TPCK), N-tosyl-L-lysylchloromethyl ketone (TLCK) or partly by N-tosyl-L-arginine methyl ester (TAME), added simultaneously with CAM, or up to 30 min after exposure to CAM, at their respective concentrations known to inhibit proteases. The protective effect of these protease inhibitors on DNA degradation cannot be due to the suppression of cell progression through S phase because cells still replicate DNA in their presence, albeit at a reduced rate. Furthermore, TPCK and TLCK protect rat thymocytes against endonucleolysis induced by prednisolone. In the latter cell system, (considered a classic model of apoptosis), endonucleolysis, which primarily affects G0/G1 cells, is unrelated to cell progression through S phase. The present data suggest that the endonucleolysis and proteolysis which accompany apoptotic cell death are coupled, and the proteolytic step is needed for DNA degradation to occur.

Animals↗
PubMed1979

Specific changes in the surface glycoprotein pattern of human promyelocytic leukemic cell line HL-60 during morphologic and functional differentiation.

The human promyelocytic leukemia cell line HL-60 can be induced to undergo morphological and functional differentiation in vitro by various low molecular weight compounds. The cellular morphology changes from blastoid appearance to that of granulocytes and the cells acquire the ability to phagocytize. We here report that the surface glycoproteins specifically change during this differentiation, as shown by the neuraminidase/galactose oxidase/NaB3H4 surface-labeling technique followed by polyacrylamide slab gel electrophoresis. The most prominent change is the loss of the major glycoprotein band typical for the blast cells which has an apparent molecular weight of 160,000 and the appearance of a major surface glycoprotein band with an apparent molecular weight of 130,000. Expression of the 130,000 molecular weight band correlates with the appearance of phagocytic and chemotactic activities of the cells. It has the same molecular weight as the major surface glycoprotein of freshly isolated human blood granulocytes.

Cell Differentiation↗
PubMed1992

The glycoprotease of Pasteurella haemolytica A1 eliminates binding of myeloid cells to P-selectin but not to E-selectin.

HL-60 cells and neutrophils treated with the glycoprotease from Pasteurella haemolytica A1, an enzyme which is specific for O-sialoglycoproteins, were found to be incapable of binding P-selectin but still bound E-selectin. Comparative analysis of [35-S] cysteine labeled proteins from HL-60 cells by 2-dimensional electrophoresis indicated that two major proteins with M(r) 100 and 115 kd were significantly removed from cells which had been treated.

Antigens, CD↗
PubMed1992

Recombinant human G-CSF and retinoic acid in synergistically inducing granulocyte differentiation of human promyelocytic leukemic cells.

The effects of recombinant human G-CSF (rhG-CSF) and retinoic acid (RA) were studied on the proliferation and differentiation of HL-60 cells and human acute myeloid leukemic cells. Synergistic effect on granulocyte differentiation was observed when HL-60 cells and primary acute promyelocytic leukemic cells were cocultured with RA plus rhG-CSF. rhG-CSF combined with RA increased more significantly the percentage of mature cells than RA alone and greatly increased NBT reduction activity (P < 0.001). These results suggested that proliferated effect of rhG-CSF on leukemic cells may be important for inducing differentiation of myeloid leukemic cells. But this effect might expose the patients to the risk of acute myeloblastic leukemia if G-CSF was used alone. However, RA could not only rule out the latter situation but retain former merit as well. The authors suggest that the combined use of G-CSF with RA is probably a new approach to the treatment of leukemia.

Cell Differentiation↗
PubMed1979

Induction of terminal differentiation in human promyelocytic leukemia cells by tumor-promoting agents.

Human promyelocytic leukemia cells (HL-60) were induced to differentiate into mature cells by the tumor-promoting agent phorbol-12-myristate-13-acetate and other related phorbol diesters. Differentiation was determined by an increase in the percent of myelocytes, metamyelocytes, and other mature myeloid cells as well as by an increase in the percent of phagocytizing cells. Induction of differentiation could be determined after 2 days of treatment with phorbol-12-myristate-13-acetate at a dose as low as 6 X 10(11) M. A correlation was found between reported tumor-promoting activity of a series of phorbol esters and their ability to induce myeloid differentiation and to inhibit cell growth. It is suggested that tumor-promoting agents like chemicals that induce terminal differentiation in these cells, at extremely low concentrations, may be used as a tool in the study of the control of cell growth, cell differentiation, and malignancy in human leukemic cells.

Cell Differentiation↗
PubMed1992

Study of the activities of Chinese herb Viscum alniformosanae Part II: The components of conditioned medium produced by Viscum alniformosanae-stimulated mononuclear cells.

The human promyelocytic cell line HL-60 can be induced to monocytoid terminal differentiation by several conditioned media produced by lectin-stimulated mononuclear cells. We reported previously that a 572-conditioned medium (CM) secreted from viscum alniformosanae-stimulated mononuclear cells also had the capacity of inducing HL-60 leukemic cells into mature monocytes. In the present study, we showed that 572-CM did not contain IFN-r, TNF, IL-1 and IL-2 as determined by using ELISA tests. This CM was unable to induce granulocyte-macrophage colony formation. Sodium dodecyl sulphate polyacrylamide gel electrophoresis (SDS-PAGE) was used to detect the components of this CM. After running the acrylamide gels, a wide band protein, in the 65-80 kd range was obtained and it was different from those of other mitogens.

Cell Differentiation↗
PubMed1978

Terminal differentiation of human promyelocytic leukemia cells induced by dimethyl sulfoxide and other polar compounds.

A human leukemic cell line (designated HL-60) has recently been established from the peripheral blood leukocytes of a patient with acute promyelocytic leukemia. This cell line displays distinct morphological and histochemical commitment towards myeloid differentiation. The cultured cells are predominantly promyelocytes, but the addition of dimethyl sulfoxide to the culture induces them to differentiate into myelocytes, metamyelocytes, and banded and segmented neutrophils. All 150 clones developed from the HL-60 culture show similar morphological differentiation in the presence of dimethyl sulfoxide. Unlike the morphologically immature promyelocytes, the dimethyl sulfoxide-induced mature cells exhibit functional maturity as exemplified by phagocytic activity. A number of other compounds previously shown to induce erythroid differentiation of mouse erythroleukemia (Friend) cells can induce analogous maturation of the myeloid HL-60 cells. The marked similarity in behavior of HL-60 cells and Friend cells in the presence of these inducing agents suggests that similar molecular mechanisms are involved in the induction of differentiation of these human myeloid and murine erythroid leukemic cells.

Butyrates↗
PubMed2025

Extracellular Vesicles Profiling in Acute Myeloid Leukemia Cell Lines: A Proteomic Characterization.

Extracellular vesicles (EVs) express features of parental cells and are fundamental in modulating the crosstalk between cancer cells and their environment. Increasing evidence suggests that EVs have a pivotal role in tumorigenesis, cancer development, and drug resistance. EVs are also involved in controlling the communication between hematopoietic stem cells and the surrounding microenvironment in the bone marrow (BM), during several processes such as self-renewal, mobilization, and lineage differentiation. Proteins expressed in cancer cell-derived EVs can be useful to further understand the regulation of hematopoietic stem cell fate, a fundamental mechanism in acute myeloid leukemia (AML). Furthermore, EVs are implicated in transmitting drug-resistance mechanisms in solid and not-solid cancer types. Here, using a proteomic approach, we analyze and validate the protein profile of EVs from three AML cell lines with different genotypes, namely OCI-AML-2, OCI-AML-3, and HL-60. The majority of the identified proteins were significantly enriched in the Gene Ontology category 'Extracellular Exosome'. Network model analysis of EV proteins revealed several significantly modulated pathways, including inflammation activation and metastatic processes in AML cell-derived EVs. The EVs proteomic profiling allows us to identify the EVs-associated molecules and pathways that could impact cancer progression and drug resistance.

Humans↗