Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The murine epithelial cell line MMC-E was used to study changes in the cytoskeletal organization associated with viral transformation of epithelial cells by two different viruses. The cells were transformed with Moloney mouse sarcoma virus (MSV) or murine leukemia virus (MuLV). The expression of actin, myosin and of intermediate filament proteins in the cells was then studied. In MMC-E cells actin and myosin were organized as belt-like structures at the edges of the border cells of the cell islands and also circumferentially in the cells inside the islands. The major change after transformation was the decrease of the actomyosin containing belt extending from cell to cell at the borders of the cell islands. Both MMC-E cells and the MSV-transformed cells contained keratin as a juxtanuclear granular aggregate whereas the MuLV-transformed cells showed bright fibrillar arrays of keratin. Both virus-transformed cell lines showed enhanced vimentin-specific fluorescence and analysis of their cytoskeletal polypeptides confirmed the result. Similar molecular forms of keratin polypeptides were seen in all cells by immunoblotting. Viral transformation of MMC-E epithelial cells thus leads to different changes in their cytoskeletal organization depending on the transforming viral or cellular gene.
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PMID:Microfilaments and intermediate filaments in epithelial cells transformed by murine sarcoma or leukemia viruses. 1159 92

This study was undertaken to examine the influence of etoposide and doxorubicin on the distribution of vimentin in cells of human leukemia cell line K-562 by using immunofluorescence microscopy. The cells were cultured with 5 different doses of etoposide: 0.02, 0.2, 2, 20, 200 microM/l and three doses of doxorubicin: 0.5, 5, 10 microM/l. Changes in vimentin filaments were dependent on concentration of drugs compared to untreated control cells. Cells treated with 20 microM/l, especially with 200 microM/l etoposide were much bigger from other cells exposed to lower doses of etoposide and control cells, and their number decreased. In most control cells vimentin was seen as a ring with the increased concentration on one pole of the cells. In 20 microM/l and 200 microM/l etoposide the cells showed rather a diffuse cytoplasmic staining pattern. Vimentin filaments were organized as a dense network in cytoplasm of these cells. Immunofluorescence studies on K-562 cells treated with doxorubicin showed that cells incubated with 5 microM/l doxorubicin have much diffuse staining pattern of vimentin with delicate reticular structure and with intense staining near one pool of the cells. Addition of 10 microM/l doxorubicin to cells resulted in increasing of fluorescence staining, which appeared in the cells as enough dense network with intense staining rather in the centre of the cell.
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PMID:Estimation of changes in vimentin filaments induced by etoposide and doxorubicin in human leukemia cell line K-562 by using immunofluorescence microscopy. 1171 80

To determine the effect on gene expression of trace levels of reactive oxygen species from mitochondria, we used the mRNA differential display technique to compare gene expression in two cell lines: M15, which overexpresses mitochondrial phospholipid hydroperoxide glutathione peroxidase (mtPHGPx), in rat basophilic leukemia RBL-2H3 cells, and a control cell line, S1. We isolated 27 differentially expressed genes, including 10 previously unreported sequences. These genes included cytoskeletal proteins (beta-tubulin, nonmuscle myosin alkali light chain, and vimentin), growth or proliferation regulators [growth differentiation factor 1 (Gdf-1), Rap1a, and inhibitor of growth 3 (Ing3)], and others. Although the expression of most of the isolated genes did not respond to ROS (hydrogen peroxide) or antioxidant (pyrolidine dithiocarbamate) treatment, the expression of Gdf-1 was downregulated by hydrogen peroxide treatment. Thus, low levels of ROS produced in mitochondria during normal cellular metabolism can modulate gene expression.
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PMID:Alteration of gene expressions by the overexpression of mitochondrial phospholipid hydroperoxide glutathione peroxidase (mtPHGPx). 1283 38

An anaplastic thyroid cancer cell line, Thena, was recently established in our laboratory following radical thyroidectomy of a patient with anaplastic thyroid cancer. Microscopically, Thena cells were spindle-shaped or small round cells. Thena cells were reactive with cytokeratin AE1/AE3 antibodies, epithelial membrane antigen, interleukin (IL)-6, epithelial growth factor receptor, transforming growth factor (TGF)-alpha, vascular endothelial growth factor, and vimentin. Thena cells secreted high levels of IL-6, leukemia inhibitor factor (LIF), tumor necrosis factor (TNF)-alpha, and TGF-beta1 in the culture supernatants, as determined by enzyme-linked immunosorbent assay. When subcutaneously injected with Thena cells, athymic nude mice developed tumor masses in the skin within 2 weeks. Furthermore, Thena cells induced cachexia in these tumor-bearing mice. High levels of human IL-6, LIF and TGF-beta1 were detected in the mouse sera. To our knowledge, the Thena cell line is the first thyroid cancer cell line reported to induce cachexia in nude mice. This cachectic animal model is worthy of further study to explore the treatment of thyroid cancer-induced cachexia.
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PMID:Production of multiple cytokines and induction of cachexia in athymic nude mice by a new anaplastic thyroid carcinoma cell line. 1465 8

The cell nucleus contains a number of mobile subnuclear organelles involved in RNA processing, transcriptional regulation and antiviral defence like Cajal and promyelocytic leukaemia (PML) bodies. It remains an open question how these bodies translocate to specific nuclear regions within the nucleus to exert their biological function. The mobility and localisation of macromolecules in the nucleus are closely related to the dynamic organisation and accessibility of chromatin. This relation has been studied with biologically inert fluorescent particles like dextrans, polystyrene nanospheres and inactive protein crystals formed by the Mx1-YFP fusion protein or other ectopically expressed proteins like vimentin. As reviewed here, properties of the chromatin environment can be identified from these experiments that determine the mobility of Cajal and PML bodies and other supramolecular complexes.
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PMID:Mobility of multi-subunit complexes in the nucleus: accessibility and dynamics of chromatin subcompartments. 1583 Feb 42

Besides tropical spastic paraparesis/human T-cell leukemia virus type-1 (HTLV-1)-associated myelopathy, the human retrovirus HTLV-1 causes inflammatory disorders such as myositis. Although the pathogenesis of HTLV-1-associated myositis is primarily unknown, a direct effect of cytokines or viral proteins in myocytotoxicity is suspected. We have developed an in vitro cell culture model to study the interactions between primary human muscle cells and HTLV-1 chronically infected cells. When HTLV-1-infected cell lines were added to differentiated muscle cultures, cytopathic changes such as fiber shrinking were observed as early as 1 day after contact. This was accompanied by alterations in desmin and vimentin organization, occurring in the absence of muscle cell infection but with Tax-1 present in myotubes. Cytopathic changes were also observed when infected culture supernatants were added to the muscle cells. Fiber atrophy and cytoskeletal disorganization were confirmed in muscle biopsies from two HTLV-1-infected patients with myositis. Transduction of cultured muscle cells with a lentiviral vector containing the HTLV-1 Tax gene reproduced such effects in vitro. The present data indicate that the myocytotoxicity that is observed in HTLV-1-associated myopathies can be due to a direct effect of the Tax-1 protein expressed in infected inflammatory cells, in the absence of muscle cell infection.
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PMID:Muscle wasting induced by HTLV-1 tax-1 protein: an in vitro and in vivo study. 1631 74

The WT1 gene is a key player in acute myeloid leukaemia, in which it is frequently over-expressed. WT1 encodes a multifunctional zinc finger protein transcription factor, which also binds mRNA. Thus increasing evidence suggests that WT1 works both at the DNA and mRNA level, not only in the urogenital system but also in other contexts. Nuclear poly(A)(+) mRNP particles were isolated by oligo(dT) chromatography from the human acute myeloid leukemia cell lines HL60 and K562, and analysed by Western blotting and 2D minigels. MALDI-TOF demonstrated the presence of hnRNP proteins, splice factors, and unexpectedly vimentin in the mRNP fraction. WT1 was also shown to be present in nuclear mRNP particles suggesting that in leukaemia, and by extension in all cancers in which it is involved, WT1 works both at the DNA and mRNA target level.
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PMID:Presence of WT1 in nuclear messenger RNP particles in the human acute myeloid leukemia cell lines HL60 and K562. 1645 49

Microfilaments, microtubules, and intermediate filaments form the cytoskeleton. These substructures play a significant role in cell motility, transport, divisions, differentiation, tumor transformation, and apoptosis. These processes are related with changes in cell shape, in which cytoskeletal proteins take an active part. In non-muscle cells, actin is an essential constituent of microfilaments, tubulin forms microtubules, and vimentin is one of the characteristic proteins of intermediate filaments. The differentiation of cells is associated inseparably with tissue and organ formation, and the induction of malignant cell differentiation can be a method of treatment, especially in hematopoietic steam cell disease therapy. In studies on tumor cell differentiation, agents such as cytokines, retinoids, forbol esters, and vitamin D3 are the most commonly used, and results show these substances may participate in different pathways of signal transduction. Retinoids and vitamin D3 mostly affect gene transcription via nuclear receptors, whereas cytokines act through membrane receptors. The results of studies show actin, tubulin, and vimentin reorganization during the differentiation of leukemia cells, but it remains unknown whether the observed changes are the cause or the result of the differentiation process.
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PMID:[The cytoskeleton reorganization and differentiation of HL-60 and K-562 human leukemia cell lines]. 1647 77

Cranial neural crest-derived ectomesenchymal cells are multipotential progenitors that contribute to various tissue types during embryogenesis. Their potential to be expanded in culture as a monolayer and to be induced into different cell lineages in vitro has not been previously reported in detail. In this study, the ectomesenchymal cells in the first branchial arch were enzymatically isolated from the mandibular processes of BALB/c mice and were maintained in an intact state in a medium containing leukaemia inhibitory factor. Here, we first evaluated the proliferative activity of the cells after the third passage, using bromodeoxyuridine labelling and in situ hybridization of telomerase mRNA. Positive staining for expression of HNK-1, S-100 and vimentin confirmed that the population of stem cells originated from the ectomesenchyme, which did not express cytokeratin. Then we investigated the molecular and cellular characteristics of the ectomesenchymal cells during their differentiation towards neurogenic, endothelial, myogenic and odontogenic lineages. Expression of multiple lineage-specific genes and proteins was detected by utilizing a range of molecular and biochemical approaches when the cells were transferred to inductive medium. Histological and immunohistochemical analysis of the induced cells at various intervals indicated obvious phenotypic alteration and presence of specific proteins for the differentiated lineages, for example nestin, factor VIII, alpha-SMA and dentin sialophosphoprotein (DSPP), respectively. Correlatively, results of reverse transcription-PCR corroborated at mRNA level the expression of the characteristic molecules during differentiation. Therefore, it is suggested that the ectomesenchymal cells derived from the first branchial arch may represent a novel source of multipotential stem cells capable of undergoing expansion and variant differentiation in vitro.
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PMID:Proliferation and pluripotency potential of ectomesenchymal cells derived from first branchial arch. 1654 44

Degeneration of axotomized GABAergic septohippocampal neurones has been shown to be enhanced in ciliary neurotrophic factor (CNTF)-deficient mice following fimbria-fornix transection (FFT), indicating a neuroprotective function of endogenous CNTF. Paradoxically, however, the cholinergic population of septohippocampal neurones was more resistant to axotomy in these mutants. As leukaemia inhibitory factor (LIF) has been identified as a potential neuroprotective factor for the cholinergic medial septum (MS) neurones, FFT-induced responses were compared in CNTF(-/-), LIF(-/-) and CNTF/LIF double knockout mice. In CNTF(-/-) mice, FFT-induced cholinergic degeneration was confirmed to be attenuated as compared with wildtype mice. The expression of both LIF and LIF receptor beta was increased in the MS providing a possible explanation for the enhanced neuronal resistance to FFT in these animals. However, ablation of the LIF gene also produced paradoxical effects; following FFT in LIF(-/-) mice no loss of GABAergic or cholinergic MS neurones was detectable during the first postlesional week, suggesting that other efficient neuroprotective mechanisms are activated in these animals. In fact, enhanced activation of astrocytes, a source of neurotrophic proteins, was indicated by increased up-regulation of glial fibrillary acidic protein and vimentin expression. In addition, mRNA levels for neurotrophin signalling components (e.g. nerve growth factor, p75(NTR)) were differentially regulated. The positive effect on axotomized cholinergic neurones seen in CNTF(-/-) and LIF(-/-) mice as well as the increased up-regulation of astrogliose markers was abolished in CNTF/LIF double knockout animals. Our results indicate that endogenous CNTF and LIF are involved in the regulation of neuronal survival following central nervous system lesion and are integrated into a network of neurotrophic signals that mutually influence their expression and function.
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PMID:Altered neuronal responses and regulation of neurotrophic proteins in the medial septum following fimbria-fornix transection in CNTF- and leukaemia inhibitory factor-deficient mice. 1707 46


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