Human Glioma Cells (human + glioma_cell)

Distribution by Scientific Domains

Terms modified by Human Glioma Cells

  • human glioma cell line

  • Selected Abstracts


    CD95-mediated Apoptosis of Human Glioma Cells: Modulation by Epidermal Growth Factor Receptor Activity

    BRAIN PATHOLOGY, Issue 1 2002
    Joachim P. Steinbach
    The death ligands CD95L and Apo2L/TRAIL are promising investigational agents for the treatment of malignant glioma. EGFR is overexpressed in a significant proportion of malignant gliomas in vivo. Here, we report that CD95L-induced cell death is enhanced by EGFR inhibition using tyrphostine AG1478 in 7 of 12 human malignant glioma cell lines. Conversely, CD95-mediated and Apo2L-induced cell death are both inhibited by overexpression of EGFR in LN-229 cells. CD95L-induced cell death augmented by AG1478 is accompanied by enhanced processing of caspase 8. LN-229 cells overexpressing the viral caspase inhibitor, crm-A, are not sensitized to CD95L-induced cell death by AG1478, indicating that EGFR exerts its antiapoptotic properties through a caspase 8-dependent pathway. These data define a modulatory effect of EGFR-activity on death ligand-induced apoptosis and indicate that EGFR inhibition is likely to improve the efficacy of death ligand-based cancer therapies. Furthermore, it is tempting to speculate that EGFR amplification protects tumor cells from death ligand-mediated host immune responses in vivo and that EGFR's effects on death receptor-mediated apoptosis may explain the anti-tumor effects of non-cytotoxic, unarmed anti-EGFR family antibodies. [source]


    BK channels in human glioma cells have enhanced calcium sensitivity,

    GLIA, Issue 4 2002
    Christopher B. Ransom
    Abstract We have previously demonstrated the expression of large-conductance, calcium-activated potassium (BK) channels in human glioma cells. In the present study, we characterized the calcium sensitivity of glioma BK channels in excised membrane patches. Channels in inside-out patches were activated at ,60 mV by 2.1 10,6 M cytosolic Ca2+, were highly K+ -selective, and had a slope conductance of ,210 pS. We characterized the Ca2+ sensitivity of these channels in detail by isolating BK currents in outside-out patches with different free [Ca2+]i. The half-maximal voltage for channel activation, V0.5, of glioma BK currents in outside-out patches was +138 mV with 0 Ca2+/10 EGTA. V0.5 was shifted to +81 mV and ,14 mV with free [Ca2+]i of 1.5 10,7 M and 2.1 10,6 M, respectively. These results suggest that glioma BK channels have a higher Ca2+ sensitivity than that described in many other human preparations. Data obtained from a cloned BK channel (hbr5) expressed in HEK cells support the conclusion that glioma BK channels have an unusually high sensitivity to calcium. In addition, the sensitivity of glioma BK channels to the BK inhibitor tetrandrine suggests the expression of BK channel auxiliary ,-subunits by glioma cells. Expression of the auxiliary ,-subunit of BK channels by glioma cells may relate to the high Ca2+ sensitivity of glioma BK channels. GLIA 38:281,291, 2002. 2002 Wiley-Liss, Inc. [source]


    Effects of prolactin on intracellular calcium concentration and cell proliferation in human glioma cells

    GLIA, Issue 3 2002
    Thomas Ducret
    Abstract Prolactin (PRL) has several physiological effects on peripheral tissues and the brain. This hormone acts via its membrane receptor (PRL-R) to induce cell differentiation or proliferation. Using reverse transcription,polymerase chain reaction (RT-PCR) combined with Southern blot analysis, we detected PRL-R transcripts in a human glioma cell line (U87-MG) and in primary cultured human glioblastoma cells. These transcripts were deleted or not in their extracellular domains. We examined the effects of PRL on intracellular free Ca2+ concentration ([Ca2+]i) in these cells in order to improve our understanding of the PRL transduction mechanism, which is still poorly documented. [Ca2+]i was measured by microspectrofluorimetry using indo-1 as the Ca2+ fluorescent probe. Spatiotemporal aspects of PRL-induced Ca2+ signals were investigated using high-speed fluo-3 confocal imaging. We found that physiological concentrations (0.4,4 nM) of PRL-stimulated Ca2+ entry and intracellular Ca2+ mobilization via a tyrosine kinase,dependent mechanism. The two types of Ca2+ responses observed were distinguishable by their kinetics: one showing a slow (type I) and the other a fast (type II) increase in [Ca2+]i. The amplitude of PRL-induced Ca2+ increases may be sufficient to provoke several physiological responses, such as stimulating proliferation. Furthermore, PRL induced a dose-dependent increase in [3H]thymidine incorporation levels and in cellular growth and survival, detected by the MTT method. These data indicate that PRL induced mitogenesis of human glioma cells. GLIA 38:200,214, 2002. 2002 Wiley-Liss, Inc. [source]


    The effects of dynein inhibition on the autophagic pathway in glioma cells

    NEUROPATHOLOGY, Issue 1 2010
    Midori Yamamoto
    Autophagy has multiple physiological functions, including protein degradation, organelle turnover and the response of cancer cells to chemotherapy. Because autophagy is implicated in a number of diseases, a better understanding of the molecular mechanisms of autophagy is needed for therapeutic purposes, including rational design of drugs. Autophagy is a process that occurs in several steps as follows: formation of phagophores, formation of mature autophagosomes, targeting and trafficking of autophagosomes to lysosomes, formation of autolysosomes by fusion between autophagosomes and lysosomes, and finally, degradation of the autophagic bodies within the lysosomes. It has been suggested that autophagosome formation is driven by molecular motor machineries, and, once formed, autophagosomes need to reach lysosomes, enriched perinuclearly around the microtubule-organizing centre. While it is recognized that all these steps require the cytoskeletal network, little is known about the mechanisms involved. Here we assessed the role of cytoplasmic dynein in the autophagic process of human glioma cells to determine the part played by dynein in autophagy. We observed that chemical interference with dynein function led to an accumulation of autophagosomes, suggesting impaired autophagosome-lysosome fusion. In contrast, we found that overexpression of dynamitin, which disrupts the dynein complex, reduced the number of autophagosomes, suggesting the requirement of the dynein-dynactin interaction in the early membrane trafficking step in autophagosome formation. These results suggest that dynein plays a variety of crucial roles during the autophagic process in glioma cells. [source]


    Vesicle amine transport protein-1 (VAT-1) is upregulated in glioblastomas and promotes migration

    NEUROPATHOLOGY & APPLIED NEUROBIOLOGY, Issue 4 2009
    S. Mertsch
    Aim:,Diffuse invasion of single-glioma cells is the main obstacle to successful therapy of these tumours. After identifying vesicle amine transport protein-1 (VAT-1) as being upregulated in invasive human gliomas, we study its possible function in glioblastoma cell migration. Methods:,Based on data obtained from previous oligonucleotide arrays, we investigated expression of VAT-1 in glioblastoma tissue and cell lines on mRNA levels using reverse transcriptase PCR. Furthermore, we examined the amount and localization of VAT-1 protein using immunoblotting and immunohistochemistry. Using small interfering RNA technology we repressed VAT-1 expression in human glioma cell lines and analysed their migration using wound healing and transwell migration assays. Results:,Increased VAT-1 mRNA and protein levels were found in glioblastoma tissues and cell lines compared with normal human brain. Small interfering RNA-mediated VAT-1 knockdown led to significantly reduced migration of human glioma cells. Conclusions:,VAT-1 is overexpressed in glioblastomas and functionally involved in glioma cell migration, representing a new component involved in glioma invasion. [source]


    Effects of exposure to a 1950 MHz radio frequency field on expression of Hsp70 and Hsp27 in human glioma cells

    BIOELECTROMAGNETICS, Issue 4 2005
    J. Miyakoshi
    Abstract Human glioma MO54 cells were used to investigate whether radio frequency (RF) field exposure could activate stress response genes. Cells were exposed to continuous wave 1950 MHz or sham conditions for up to 2 h. Specific absorption rates (SARs) were 1, 2, and 10 W/kg. For the cell growth experiment, cell numbers were counted at 0,4 days after exposure. Expression of Hsp27 and Hsp70, as well as the level of phosphorylated Hsp27 (78Ser) protein, was determined by Western blotting. It was found that sham exposed and RF exposed cells demonstrated a similar growth pattern up to 4 days after RF field exposure. RF field exposure at both 2 and 10 W/kg did not affect the growth of MO54 cells. In addition, there were no significant differences in protein expression of Hsp27 and Hsp70 between sham exposed and RF exposed cells at a SAR of 1, 2, or 10 W/kg for 1 and 2 h. However, exposure to RF field at a SAR of 10 W/kg for 1 and 2 h decreased the protein level of phosphorylated Hsp27 (78Ser) significantly. Our results suggest that although exposure to a 1950 MHz RF field has no effect on cell proliferation and expression of Hsp 27 and Hsp70, it may inhibit the phosphorylation of Hsp27 at Serine 78 in MO54 cells. Bioelectromagnetics 26:251,257, 2005. 2005 Wiley-Liss, Inc. [source]