Antiproliferative effects induced by guanine-based purines require hypoxanthine-guanine phosphoribosyltransferase activity

2010 ◽  
Vol 391 (9) ◽  
Author(s):  
Roberta Garozzo ◽  
Maria Angela Sortino ◽  
Carlo Vancheri ◽  
Daniele Filippo Condorelli
Keyword(s):  
Cell Line ◽  
Glioma Cell Line ◽  
Inhibitory Effects ◽  
Antiproliferative Effects ◽  
Growth Inhibitory ◽  
Tumoral Cell ◽  
A Cell ◽  
Hypoxanthine Guanine Phosphoribosyltransferase ◽  
U87 Cells

Abstract Guanine (GUA), guanosine and GMP exert a marked growth inhibition on the U87 glioma cell line that is not seen with other tested nucleotides, nucleosides and nucleobases. This effect could be replicated in several different human tumoral cell lines. Guanine shows a higher potency than guanosine or GMP, and co-treatments with adenosine or adenine are able to antagonize or revert the antiproliferative effect of guanine. The loss of the guanine effect in a cell line bearing a mutated inactive hypoxanthine-guanine phosphoribosyltransferase (HGPRT), and the decreased potency of GUA in U87 cells silenced for HGPRT transcripts, demonstrates the central role of the intracellular metabolism of GUA for growth-inhibitory effects. Considering the potential application of growth-inhibitory substances in anticancer therapy, knowledge of the molecular mechanism underlying GUA-induced effects encourages studies aimed at defining possible tumoral targets for experimental therapies.

scholarly journals P01.17 * ROLE OF PHOSPHATYDILCHOLINE-SPECIFIC PHOSPHOLIPASE C IN MODULATION OF CXCL12/CXCR4 AXIS IN A HUMAN GLIOMA CELL LINE

2014 ◽  
Vol 16 (suppl 2) ◽  
pp. ii30-ii30 ◽  
Author(s):  
L. Mercurio ◽  
A. Ricci ◽  
S. Cecchetti ◽  
A. Pacella ◽  
F. Podo ◽  
...  
Keyword(s):  
Phospholipase C ◽  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line ◽  
Human Glioma ◽  
Human Glioma Cell Line ◽  
Human Glioma Cell ◽  
Cxcr4 Axis

The role of ecto-5′-nucleotidase/CD73 in glioma cell line proliferation

2008 ◽  
Vol 319 (1-2) ◽  
pp. 61-68 ◽  
Author(s):  
Luci Bavaresco ◽  
Andressa Bernardi ◽  
Elizandra Braganhol ◽  
Angélica Regina Cappellari ◽  
Liliana Rockenbach ◽  
...  
Keyword(s):  
Cell Line ◽  
Glioma Cell ◽  
Glioma Cell Line

scholarly journals Transfected leukocyte integrin CD11b/CD18 (Mac-1) mediates phorbol ester-activated, homotypic cell:cell adherence in the K562 cell line

Blood ◽  
1993 ◽  
Vol 82 (8) ◽  
pp. 2537-2545 ◽  
Author(s):  
DD Hickstein ◽  
E Grunvald ◽  
G Shumaker ◽  
DM Baker ◽  
AL Back ◽  
...  
Keyword(s):  
Cell Line ◽  
Cell Activation ◽  
Blast Crisis ◽  
K562 Cells ◽  
Myelogenous Leukemia ◽  
Cell Clones ◽  
A Cell ◽  
Neutrophil Adherence ◽  
The Individual

Abstract The CD11b/CD18 leukocyte integrin molecule mediates diverse neutrophil adherence-related functions, including cell:cell and cell:extracellular matrix attachments. To study the individual role of this leukocyte integrin in cell adherence in hematopoietic cells, we expressed the CD11b/CD18 complex on the surface of K562 cells, a cell line derived from an individual with chronic myelogenous leukemia in blast crisis. We used an amphotrophic retroviral vector designated LCD18SN, harboring the complete coding sequence for the CD18 subunit, to transfer the CD18 cDNA into K562 cells and select stable cell lines. The CD11b subunit in the expression plasmid pREP4 was transfected into these K562/CD18 cells by electroporation and stable cell clones were selected. These K562 cells possessed RNA and intracellular protein for each subunit, and they expressed the CD11b/CD18 heterodimer on the cell surface. When CD11b/CD18 expressing K562 cells were stimulated with phorbol myristate acetate (50 ng/mL) for 24 to 48 hours, these K562 cells formed dense cell:cell aggregates. This homotypic aggregation required both activation of the CD11b/CD18 complex and the induction of the counter- receptor for CD11b/CD18 on the conjugate cell. This cell line will (1) enable the structure-function relationships between cell activation and homotypic adherence to be assessed, (2) provide the opportunity to identify accessory molecules required for activation of the CD11b/CD18 complex, and (3) facilitate the identification of novel ligands for the CD11b/CD18 complex.

scholarly journals TNF-induced IL-8 and MCP-1 production in the eosinophilic cell line, EOL-1

1996 ◽  
Vol 5 (3) ◽  
pp. 218-223 ◽  
Author(s):  
L. A. Goldstein ◽  
R. M. Strieter ◽  
H. L. Evanoff ◽  
S. L. Kunkel ◽  
N. W. Lukacs
Keyword(s):  
Cell Line ◽  
Inflammatory Responses ◽  
Kinetic Studies ◽  
Inhibitory Effects ◽  
Chemokine Production ◽  
Eosinophil Cell ◽  
Tnf Α ◽  
Eosinophilic Cell ◽  
Suppressive Cytokine

The role of eosinophils in inflammation and their mode of activation is not well understood. Eosinophil accumulation and subsequent expression of cytokines at the site of inflammation may play a role in exacerbation of inflammatory responses. In the present study, we have examined the role of TNF-α in eosinophil activation and chemokine production using a human leukaemic eosinophil cell line, EOL-1. Initial studies demonstrated that TNF-α induced the upregulation of IL-8 and MCP-1 mRNA and protein. Kinetic studies indicated production of chemokines, IL-8 and MCP-1, as early as 4 h post-activation, with peak levels of chemokine produced at 8 h, and decreasing by 24 h post-TNF-α activation. When IL-10, a suppressive cytokine, was incubated with TNF-α and EOL-1 cells, no effect was observed on IL-8 and MCP-1 production. However, dexamethasone, a glucocorticoid, demonstrated potent inhibitory effects on the EOL-1-derived chemokines. These studies indicate that eosinophils may be a significant source of chemokines capable of participating in, and maintaining, leukocyte recruitment during inflammatory responses, such as asthma.

scholarly journals LncRNA SNHG14 regulates the DDP-resistance of non-small cell lung cancer cell through miR-133a/HOXB13 pathway

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Li Xu ◽  
Yan Xu ◽  
Min Yang ◽  
Jia Li ◽  
Fang Xu ◽  
...  
Keyword(s):  
Cell Line ◽  
A549 Cells ◽  
Parental Cell ◽  
Luciferase Reporter ◽  
Inhibitory Effects ◽  
Through Flow ◽  
Non Coding Rnas ◽  
Apoptosis Related Protein ◽  
Dual Luciferase Reporter Assay

Abstract Background Recently, long non-coding RNAs (lncRNAs) have been reported to be involved in regulating chemo-resistance of NSCLC, however, the role of lncRNA SNHG14 in the DDP-resistance of NSCLC remains unexplored. Methods Relative expression of SNHG14, HOXB13 and miR-133a in DDP-resistant A549 (A549/DDP) cell and its parental cell A549 were measured using qRT-PCR. Cell proliferation viability of indicated A549/DDP cell was estimated via CCK-8 and colony formation experiments. Cell cycle and apoptosis were analyzed through flow cytometry. Expression of apoptosis-related protein and HOXB13 were detected via western blot. The interaction among SNHG14, HOXB13 and miR-133a was predicted by bioinformatics and validated by dual-luciferase reporter assay. Results LncRNA SNHG14 and HOXB13 were upregulated while miR-133a was downregulated in A549/DDP cell line compared to A549 cell line. SNHG14 knockdown or miR-133a overexpression was demonstrated to increase the DDP-sensitivity of A549/DDP cells. SNHG14 was revealed to compete with HOXB13 for miR-133a binding in A549/DDP cells. Inhibition of miR-133a in A549 cells could reverse the promotive effects of SNHG14 knockdown on DDP-sensitivity, as well as the inhibitory effects on HOXB13 expression. HOXB13 overexpression was revealed to abolish the enhanced effects of miR-133a on the sensitivity of A549/DDP cell to DDP. Conclusion Our findings demonstrated that SNHG14 was involved in the development of DDP-resistance of A549/DDP cells through miR-133a/HOXB13 axis, which may present a path to novel therapeutic stratagems for DDP resistance of NSCLC.

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