Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11441
Title: The expression of calcitonin receptor detected in malignant cells of the brain tumour glioblastoma multiforme and functional properties in the cell line A172.
Authors: Wookey, Peter J;McLean, Catriona A;Hwang, Peter;Furness, Sebastian G B;Nguyen, Sandy;Kourakis, Angela;Hare, David L;Rosenfeld, Jeffrey V
Affiliation: Department of Medicine/Cardiology, University of Melbourne, Lance Townsend Building, Level 10, Austin Campus, Austin Health, Studley Road, Heidelberg, Vic. 3084, Australia. pwookey@unimelb.edu.au
Issue Date: 15-Feb-2012
Citation: Histopathology 2012; 60(6): 895-910
Abstract: Previous studies have indicated that expression of calcitonin receptor (CTR) could be induced in a proinflammatory environment. In the present study, CTR-immunoreactivity (CTR-ir) was investigated in brain tissue from patients with glioblastoma multiforme (GBM).In immunohistochemical analysis of GBM samples, tissues with complex glomeruloid structures surrounded by malignant cells were analysed for CTR-ir using anti-human CTR antibodies generated against two separate epitopes of CTR. CTR-ir was associated predominantly with glial cells. Regions with CTR-ir cells were found in 12 of 14 GBM tumours (P < 0.05). Using confocal microscopy, CTR-ir cells were identified that were also positive for glial fibrillary acidic protein, nestin and CD133. Antibodies were verified using immunoblots and confocal microscopy of the Cercopithecus aethiops(COS)-7 transfectants. Immunoblots of membrane preparations from the CTR-positive cell lines demonstrated a major band (≈ 67 kDa) and minor band (≈ 52 kDa), but the intensity was reversed for the GBM cell line A172. In cultured A172 cells, functional studies demonstrated calcitonin stimulation of adenylyl cyclase and inhibition of extracellular-regulated kinase (ERK)1/2 phosphorylation.The findings that (i) CTR was expressed by glioma cells in a majority of GBM tumours tested, (ii) CTR(+) /CD133(+) cells were identified and (iii) second messenger systems were functionally modified by calcitonin in A172 cells suggest that CTR might be a useful therapeutic target in GBM.
Internal ID Number: 22335784
URI: http://ahro.austin.org.au/austinjspui/handle/1/11441
DOI: 10.1111/j.1365-2559.2011.04146.x
URL: http://www.ncbi.nlm.nih.gov/pubmed/22335784
Type: Journal Article
Subjects: 3T3 Cells
Adenylate Cyclase.metabolism
Animals
Antigens, CD.metabolism
Brain Neoplasms.drug therapy.metabolism.pathology
Cell Line, Tumor
Cercopithecus aethiops
Glioblastoma.drug therapy.metabolism.pathology
Glycoproteins.metabolism
Humans
Immunoblotting
Immunohistochemistry
MAP Kinase Signaling System
Mice
Peptides.metabolism
Receptors, Calcitonin.metabolism
Second Messenger Systems
Transfection
Tumor Markers, Biological.metabolism
Appears in Collections:Journal articles

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