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Brain Tumor Cells (brain + tumor_cell)
Selected AbstractsSelective Inhibition of Human Brain Tumor Cells through Multifunctional Quantum-Dot-Based siRNA Delivery,ANGEWANDTE CHEMIE, Issue 1 2010Jongjin Jung Auf den Punkt gebracht: Quantenpunkte (QDs), die mit thiolmodifizierter small interfering RNA (siRNA) konjugiert sind, wurden mit thiolmodifizierten RGD- und HIV-Tat-Peptiden funktionalisiert. Diese multifunktionellen QDs wurden für den zielgerichteten Transport und die Verfolgung von siRNA-Molekülen zum Knockdown des für EGFRvIII kodierenden Gens genutzt, was zur Herunterregulierung des PI3K-Akt-Signalwegs und zur Apoptose maligner Gehirntumorzellen führte. [source] ,v -Integrin antagonist EMD 121974 induces apoptosis in brain tumor cells growing on vitronectin and tenascinINTERNATIONAL JOURNAL OF CANCER, Issue 5 2002Takashi Taga Abstract Orthotopic brain tumor growth is inhibited in athymic mice by the daily systemic administration of the ,v -integrin antagonist EMD 121974. This compound, a cyclic RGD-penta-peptide, is a potent inhibitor of angiogenesis, which induces apoptosis of growing endothelial cells through inhibition of their ,v -integrin interaction with the matrix proteins vitronectin and tenascin. Here we show that EMD 121974 also induces apoptosis in the ,v -integrin-expressing tumor cell lines U87 MG and DAOY by detaching them from vitronectin and tenascin, matrix proteins known to be essential for brain tumor growth and invasion. These matrix proteins are shown to be produced by the brain tumor cells in vitro and in vivo. Furthermore, only tumor cells expressing ,v -integrins responded to the treatment with EMD 121974, after xenotransplantation into the forebrain of nude mice, supporting the importance of tumor cell-matrix interactions in tumor cell survival in the brain. Thus, the ,v -antagonist EMD 121974 suppresses brain tumor growth through induction of apoptosis in both brain capillary and brain tumor cells by preventing their interaction with the matrix proteins vitronectin and tenascin. The dual action of this peptide explains its potent growth suppression of orthotopically transplanted brain tumors. © 2002 Wiley-Liss, Inc. [source] The natural compound n -butylidenephthalide derived from Angelica sinensis inhibits malignant brain tumor growth in vitro and in vivo3JOURNAL OF NEUROCHEMISTRY, Issue 4 2006Nu-Man Tsai Abstract The naturally-occurring compound, n -butylidenephthalide (BP), which is isolated from the chloroform extract of Angelica sinensis (AS-C), has been investigated with respect to the treatment of angina. In this study, we have examined the anti-tumor effects of n -butylidenephthalide on glioblastoma multiforme (GBM) brain tumors both in vitro and in vivo. In vitro, GBM cells were treated with BP, and the effects of proliferation, cell cycle and apoptosis were determined. In vivo, DBTRG-05MG, the human GBM tumor, and RG2, the rat GBM tumor, were injected subcutaneously or intracerebrally with BP. The effects on tumor growth were determined by tumor volumes, magnetic resonance imaging and survival rate. Here, we report on the potency of BP in suppressing growth of malignant brain tumor cells without simultaneous fibroblast cytotocixity. BP up-regulated the expression of Cyclin Kinase Inhibitor (CKI), including p21 and p27, to decrease phosphorylation of Rb proteins, and down-regulated the cell-cycle regulators, resulting in cell arrest at the G0/G1 phase for DBTRG-05MG and RG2 cells, respectively. The apoptosis-associated proteins were dramatically increased and activated by BP in DBTRG-05MG cells and RG2 cells, but RG2 cells did not express p53 protein. In vitro results showed that BP triggered both p53-dependent and independent pathways for apoptosis. In vivo, BP not only suppressed growth of subcutaneous rat and human brain tumors but also, reduced the volume of GBM tumors in situ, significantly prolonging survival rate. These in vitro and in vivo anti-cancer effects indicate that BP could serve as a new anti-brain tumor drug. [source] Cytotoxicity and apoptosis enhancement in brain tumor cells upon coadministration of paclitaxel and ceramide in nanoemulsion formulationsJOURNAL OF PHARMACEUTICAL SCIENCES, Issue 7 2008Ankita Desai Abstract The objective of this study was to examine augmentation of therapeutic activity in human glioblastoma cells with combination of paclitaxel (PTX) and the apoptotic signaling molecule, C6 -ceramide (CER), when administered in novel oil-in-water nanoemulsions. The nanoemulsions were formulated with pine-nut oil, which has high concentrations of essential polyunsaturated fatty acid (PUFA). Drug-containing nanoemulsions were characterized for particle size, surface charge, and the particle morphology was examined with transmission electron microscopy (TEM). Epi-fluorescent microscopy was used to analyze nanoemulsion-encapsulated rhodamine-labeled PTX and NBD-labeled CER uptake and distribution in U-118 human glioblastoma cells. Cell viability was assessed with the MTS (formazan) assay, while apoptotic activity of PTX and CER was evaluated with caspase-3/7 activation and flow cytometry. Nanoemulsion formulations with the oil droplet size of approximately 200 nm in diameter were prepared with PTX, CER, and combination of the two agents. When administered to U-118 cells, significant enhancement in cytotoxicity was observed with combination of PTX and CER as compared to administration of individual agents. The increase in cytotoxicity correlated with enhancement in apoptotic activity in cells treated with combination of PTX and CER. The results of these studies show that oil-in-water nanoemulsions can be designed with combination therapy for enhancement of cytotoxic effect in brain tumor cells. In addition, PTX and CER can be used together to augment therapeutic activity, especially in aggressive tumor models such as glioblastoma. © 2007 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci 97:2745,2756, 2008 [source] | ||||||||||