Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0265264 (HOS)
1,119 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our previous experiments have indicated that the antitumor effects of a polyamine biosynthetic inhibitor, methylglyoxal bis(cyclopentylamidinohydrazone) (MGBCP), on human osteosarcoma cell lines such as MG-63, G-292 and HOS cells are obtained by its action depleting the cellular polyamine contents. In the present study, the effects of polyamine depletion by MGBCP on the cell cycle progression in these osteosarcoma cell lines were investigated by flow cytofluormetric analysis. MGBCP arrested the tumor cells at the G1 phase by preventing the G/S phase transition. Mitotic indexes (MIs) in these MGBCP-inhibited tumor cells were also decreased. These findings suggest that MGBCP suppresses the cell cycle progression in osteosarcoma MG-63, G-292 and HOS cells by inhibiting intracellular polyamine biosynthesis.
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PMID:Effects of methylglyoxal bis (cyclopentylamidinohydrazone) (MGBCP) on cell cycle progression in three human osteosarcoma cell lines. 891 52

We investigated whether stromal cells obtained from human tonsils could interact and modulate the proliferation of the osteosarcoma cell in order to determine why lymph node metastases usually have a low incidence and remain occult using routine examinations. The effects of the supernatant of resting or activated stromal cells were analysed on osteoblastic cell proliferation of three different cell lines (HOS, U2, OS, MG-63). Only the proliferation of MG-63 was significantly inhibited. The direct adhesion of stromal cells to the osteosarcoma cell lines caused a greater inhibition of the proliferation of all three lines tested.
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PMID:Effect of stromal cells from human lymph nodes on the growth of osteosarcoma cell lines. 896 96

Alkaline phosphatase (ALP) plays an important role in bone mineralization; high levels in differentiated osteoblasts allows their identification easily in vitro. It is generally assumed that the activity of ALP in osteosarcoma-derived cell lines commonly used in studies of bone cell biology is exclusively due to the bone/liver/kidney (BLK) isoenzyme. However, we noted that two human osteosarcoma cell lines, U-2 OS and U-393 OS, predominantly expressed a truncated 1.8 kb mRNA for BLK-ALP. This observation stimulated further investigation upon the ability of ALP to form functional protein. We found that, unlike the BLK-ALP of the Saos-2 osteosarcoma cell line, the activity of U-2 OS ALP was thermostable, unaffected by L-homoarginine and levamisole, but inhibited by L-phenylalanine; these properties are characteristic of the placental and/or placental-like (PL-/PL-like ALP) isoenzymes which are 98% homologous at the amino acid level. In the U-393 OS cell line, which expresses the normal-sized 2.5 kb mRNA in substantially higher levels than that produced by U-2 OS cells, the ALP activity had kinetic properties very similar to that produced by the Saos-2 line for all criteria tested. The HOS osteosarcoma cell line (also known as TE-85), which express the normal-sized 2.5 kb BLK-ALP mRNA only, exhibited ALP activity with kinetic properties of both the BLK and PL-/PL-like isoenzymes. The three test lines, U-2 OS, U-393 OS and HOS, produced PL-/PL-like ALP mRNA and protein constitutively, and levels of these increased in cells treated with 1 microM dexamethasone. However, dexamethasone treatment of cells did not alter the types of ALP isoenzyme expressed. Thus our results show that, like Saos-2 cells, U-393 OS cells produce active BLK-ALP exclusively, whereas U-2 OS cells produce PL-/PL-like ALP only, and the HOS cell line produces both. Our findings have important implications for phenotypic characterization of various human osteosarcoma cell lines, and suggest that the production of PL-/PL-like ALP may be a more common occurrence in osteosarcomas than was originally thought.
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PMID:Constitutive expression of non-bone/liver/kidney alkaline phosphatase in human osteosarcoma cell lines. 899 82

In order to investigate the subnuclear interactions of the WT1 gene product, nuclear fractionation analyses were performed with human osteosarcoma HOS and myelogenous leukemia K562 cells. The WT1 protein was tightly associated with the nucleus and was resistant to high-salt or detergent extraction and DNase I digestion. Both the expression level and stability of WT1 and its resistance to high salt and DNase I treatments remained constant during the cell cycle. In addition, human WT1 ectopically expressed in mouse NIH3T3 cells was also resistant to these treatments. These results suggest that WT1 functions in tight association with the nuclear matrix.
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PMID:The Wilms tumor protein is persistently associated with the nuclear matrix throughout the cell cycle. 920 4

To investigate the functional differences between estrogen receptor (ER) alpha and beta subtypes, we studied the expression and the transcription stimulating activities of these receptors. RT-PCR has demonstrated that ER alpha is expressed at a high level in MCF-7 cells derived from human breast cancer. Both ER alpha and ER beta were expressed at a lower level in HOS-TE85 and Saos2 cells derived from human osteosarcoma. Chloramphenicol acetyltransferase reporter assay detected the transcriptional activation by the endogenous receptor only in MCF-7 cells. Agonistic effect of tamoxifen was observed as strong as that of 17beta-estradiol on ERE activation in MCF-7 cells at the concentration of 10(-7) M when ERE-containing reporter is constructed with beta-globin promoter. The effect of tamoxifen was not apparent when the reporter was constructed with thymidine kinase promoter, suggesting that the differential gene activation between tamoxifen and estrogen may take place depending upon ERE-promoter context. Agonistic activity of tamoxifen was also detected in COS-7 and Saos-2 cells, but not in HEC-1 cells derived from human endometrial carcinoma via exogenously expressed ER. Interestingly, this effect was ER alpha specific. Thus, we demonstrate that agonistic effect of tamoxifen depends on the cell type, ERE-promoter context, and ER subtype. These parameters would explain at least a part of the tissue specific effects of antiestrogens in vivo.
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PMID:Agonistic effect of tamoxifen is dependent on cell type, ERE-promoter context, and estrogen receptor subtype: functional difference between estrogen receptors alpha and beta. 922 41

The CD95/APO-1 Fas receptor/ligand system plays a crucial role in growth control by mediating apoptosis in lymphoid and non-lymphoid cells. To investigate the role of CD95-mediated apoptosis in osteosarcoma, we studied 3 human osteosarcoma cell lines (HOS/TE 85, MG 63 and Saos-2) and osteoblasts derived from bone biopsies. In contrast to osteoblast-like cells, all cell lines were resistant to anti-APO-1-induced apoptosis despite constitutive CD95 expression at intermediate levels. Blocking of macromolecular synthesis by cycloheximide or actinomycin D or modulation of CD95 expression by cytokines (TNF-alpha and/or gamma-interferon) restored sensitivity to anti-APO-1-induced cell death. PCR analysis of the CD95 transcripts revealed the production of a truncated splice variant that codes for a soluble form of the CD95 receptor. Synthesis and secretion of soluble CD95 protein into the culture supernatant was demonstrated by Western blot analysis. Treatment with sensitizing cytokines led to up-regulation of full-length CD95 transcripts and the encoded membrane-bound CD95 protein but not the truncated mRNA splice variant and the corresponding soluble receptor, as shown by PCR and Western blot analysis. The biological activity of soluble CD95 secreted by osteosarcoma cells was demonstrated by the ability of osteosarcoma supernatants to protect the sensitive T-cell line Jurkat from anti-APO-1-mediated apoptosis. Our results suggest that the production of soluble CD95 by osteosarcoma cell lines that may block physiological death signals and the production of membrane-bound CD95 are differently regulated by cytokines via modulation of RNA splicing.
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PMID:Modulation of resistance to anti-APO-1-induced apoptosis in osteosarcoma cells by cytokines. 924 1

Recently we found that primary human osteoblast-like cells (HOBs) support hematopoietic progenitor cells (assayed by colony formation in methylcellulose) and long-term culture initiating (LTC-IC) activity in vitro. In the present investigation, we evaluate whether human osteosarcoma cells share in these activities. We observed that relative to controls, significantly fewer hematopoietic colonies were formed in the presence of HOS TE85, MG-63, SaOS-2, or U2-OS human osteosarcomas. In addition, neither MG-63 or SaOS-2 cells supported hematopoietic progenitor cell activity or LTC-IC activity in vitro. We established that the suppressive activity produced by the osteosarcomas is soluble, correlated with osteosarcoma cell number and is partially neutralized with antibody to TGF-beta 1,2,3. While it is clear that the osteosarcomas express several phenotypic characteristics of primary human osteoblasts, these data suggest that they may be functionally disregulated with regard to their ability to support normal hematopoiesis. For these reasons, caution should be exercised when evaluating osteoblastic and hematopoietic cell interactions based purely on the use of osteosarcoma cell lines.
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PMID:Human osteosarcomas inhibit hematopoietic colony formation: partial reversal by antibody to transforming growth factor-beta 1. 931 39

Metastatic osteosarcoma is a potential target for gene therapy, because conventional therapies are only palliative and metastatic disease is invariably fatal. Overexpression of the cyclin G1 (CYCG1) gene is frequently observed in human osteosarcoma cells, and its continued expression is found to be essential for their survival. Previously, we reported that down-regulation of cyclin G1 protein expression induced cytostatic and cytocidal effects in human MG-63 osteosarcoma cells (Skotzko et al., Cancer Research, 1995). Here, we extend these findings in a tumorigenic MNNG/HOS cell line and report on the effective inhibition of tumor growth in vivo by an antisense cyclin G1 retroviral vector when delivered as concentrated high titer vector supernatants directly into rapidly growing subcutaneous tumors in athymic nude mice. Histologic sections from the antisense cyclin G1 vector-treated tumors showed decreased mitotic indices and increased stroma formation within the residual tumors. Furthermore, in situ analysis of the cell-cycle kinetics of residual tumor cells revealed a decrease in the number of cells in S and G2/M phases of the cell cycle concomittant with an accumulation of cells in the G1 phase. Taken together, these studies demonstrate in vivo efficacy of a high-titer antisense cyclin G1 retroviral vector in an animal model of osteosarcoma.
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PMID:Retroviral vector-mediated transfer of an antisense cyclin G1 construct inhibits osteosarcoma tumor growth in nude mice. 932 69

In human periosteum-derived osteoblastic cells (SaM-1) and human osteosarcoma-derived cells (SaOS-2, HOS, MG-63), the mRNA expressions of calcitonin gene-related peptide receptor (CGRP-R), substance P receptor (SP-R), neuropeptide Y receptor (NPY-R), beta-adrenergic receptors (beta1-R, beta2-R, beta3-R), vasoactive intestinal polypeptide type 1 and type 2 receptors (VIP-1R, VIP-2R) and pituitary adenylate cyclase activating polypeptide receptor (PACAP-R) were examined by reverse transcription-polymerase chain reaction (RT-PCR). According to the magnitude of the mRNA expression of alkaline phosphatase (ALP), the relative state of commitment of these osteoblastic cell lines to the osteoblast lineage was SaM-1 > SaOS-2 > HOS > MG-63. CGRP-R, NPY-R, VIP-1R and beta2-R, but not SP-R, VIP-2R, PACAP-R, beta1-R and beta3-R, were expressed in osteoblasts as well as osteosarcoma cells. Expression of these receptors seems to be a common feature in osteoblastic cells, but the magnitude of expression was not dependent upon the relative state of commitment of the osteoblastic cells to the osteoblast lineage. In addition, VIP mRNA was not expressed in osteoblastic cells, suggesting the absence of an autocrine system of VIP in osteoblasts. These observations suggest that these neuropeptides and norepinephrine are involved in local regulation of human bone metabolism.
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PMID:Expression of mRNAs for neuropeptide receptors and beta-adrenergic receptors in human osteoblasts and human osteogenic sarcoma cells. 935 Aug 48

Bone is an estradiol-responsive tissue. Estrogen withdrawal during the menopause causes loss of bone mass and clinically relevant osteoporosis in a third of all women. Sufficient or impaired local production, as well as degradation of estradiol in cells present in the bone microenvironment might be an important mechanism of rescue or might contribute to the development of osteoporosis, respectively. We therefore investigated aromatase and 17beta-hydroxysteroid dehydrogenase type IV (17beta-HSD IV) expression in osteoblast- and osteoclast-like cells. Aromatase mRNA was increasingly expressed in myeloid THP 1 cells differentiated along the monocyte/phagocyte pathway exploiting vitamin D and either granulocyte-macrophage-stimulating factor (GMCSF) or macrophage-stimulating factor (MCSF). In long-term cultures, when sequentially exposed to vitamin D (days 0-21) and GMCSF (days 5-10) and plated on collagen, the amount of expression of aromatase mRNA steadily increased along with the increasing expression of osteopontin mRNA, alpha(v) integrin mRNA, c-fms (MCSF-receptor) mRNA and multinucleated cells developing. The conversion of estradiol from testosterone (10(-7) M/l) in the supernatants of dishes mirrored changes in aromatase mRNA expression and by day 21 rose to 30,000 ng/10(7) cells/24 h. 17Beta-HSD IV mRNA expression was abundant in undifferentiated THP 1 cells and was decreased to approximately 50% by day 21. Unstimulated SV-40 immortalized fetal osteoblasts did not express aromatase mRNA, but the expression was stimulated by the addition of the phorbol ester phorbol myristate acetate (PMA). Unstimulated osteoblasts from primary cultures did not express aromatase mRNA. Osteoblast-like osteosarcoma cells MG 63 expressed faint levels of aromatase mRNA in contrast to the osteosarcoma cell line HOS 58. 17Beta-HSD IV mRNA was expressed in fetal osteoblasts as well as in osteoblasts from primary culture, MG 63 and HOS 58 cells. In summary, we can show the expression of estradiol metabolizing enzymes in cells which are present in the bone microenvironment. Impaired aromatase expression and/or enhanced expression of 17beta-HSD IV may contribute to the pathogenesis of osteoporosis.
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PMID:Local estradiol metabolism in osteoblast- and osteoclast-like cells. 936 87


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