Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells

<p>Abstract</p> <p>Background</p> <p>The peptide hormone calcitonin (CT) can significantly effect the proliferation rate of CT receptor (CTR) positive human cancer cells. We wish to identify additional human cancers expressing CTRs and assay the effects of CT on their g...

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Main Authors: Pondel Marc D, Mould Richard
Format: Article
Language:English
Published: BMC 2003-04-01
Series:Cancer Cell International
Online Access:http://www.cancerci.com/content/3/1/6
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spelling doaj-90effcdf7a34405f9ad83751e0044b902020-11-24T22:10:05ZengBMCCancer Cell International1475-28672003-04-0131610.1186/1475-2867-3-6Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cellsPondel Marc DMould Richard<p>Abstract</p> <p>Background</p> <p>The peptide hormone calcitonin (CT) can significantly effect the proliferation rate of CT receptor (CTR) positive human cancer cells. We wish to identify additional human cancers expressing CTRs and assay the effects of CT on their growth rates and signal transduction pathways.</p> <p>Results</p> <p>The expression of the human calcitonin receptor (hCTR) gene in the chronic myelogenous leukemia cell line K562 was examined. RT-PCR on total RNA extracted from K562 cells detected the presence of hCTR mRNA. Further analysis demonstrated that multiple hCTR isoforms were present. Incubation of K562 cells with salmon calcitonin (sCT), but not amylin, caused an increase in intracellular levels of cAMP similar to that induced by forskolin treatment. We further demonstrated that butyrate induced erythroid differentiation of K562 cells caused a significant decrease in hCTR mRNA levels. However, phorbol myristate acetate (PMA) induced megakaryocytic differentiation of these cells had no significant effect on hCTR mRNA levels. We demonstrated that exposure to various concentrations of sCT had no effect on the cellular proliferation of K562 cells <it>in vitro</it>.</p> <p>Conclusion</p> <p>Chronic myelogenous k562 cells express multiple CTR isoforms. However, CT does not effect K562 proliferation rates. It is likely that the small increase in intracellular levels of cAMP following CT treatment is not sufficient to interfere with cellular growth.</p> http://www.cancerci.com/content/3/1/6
collection DOAJ
language English
format Article
sources DOAJ
author Pondel Marc D
Mould Richard
spellingShingle Pondel Marc D
Mould Richard
Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells
Cancer Cell International
author_facet Pondel Marc D
Mould Richard
author_sort Pondel Marc D
title Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells
title_short Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells
title_full Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells
title_fullStr Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells
title_full_unstemmed Calcitonin receptor gene expression in K562 chronic myelogenous leukemic cells
title_sort calcitonin receptor gene expression in k562 chronic myelogenous leukemic cells
publisher BMC
series Cancer Cell International
issn 1475-2867
publishDate 2003-04-01
description <p>Abstract</p> <p>Background</p> <p>The peptide hormone calcitonin (CT) can significantly effect the proliferation rate of CT receptor (CTR) positive human cancer cells. We wish to identify additional human cancers expressing CTRs and assay the effects of CT on their growth rates and signal transduction pathways.</p> <p>Results</p> <p>The expression of the human calcitonin receptor (hCTR) gene in the chronic myelogenous leukemia cell line K562 was examined. RT-PCR on total RNA extracted from K562 cells detected the presence of hCTR mRNA. Further analysis demonstrated that multiple hCTR isoforms were present. Incubation of K562 cells with salmon calcitonin (sCT), but not amylin, caused an increase in intracellular levels of cAMP similar to that induced by forskolin treatment. We further demonstrated that butyrate induced erythroid differentiation of K562 cells caused a significant decrease in hCTR mRNA levels. However, phorbol myristate acetate (PMA) induced megakaryocytic differentiation of these cells had no significant effect on hCTR mRNA levels. We demonstrated that exposure to various concentrations of sCT had no effect on the cellular proliferation of K562 cells <it>in vitro</it>.</p> <p>Conclusion</p> <p>Chronic myelogenous k562 cells express multiple CTR isoforms. However, CT does not effect K562 proliferation rates. It is likely that the small increase in intracellular levels of cAMP following CT treatment is not sufficient to interfere with cellular growth.</p>
url http://www.cancerci.com/content/3/1/6
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AT mouldrichard calcitoninreceptorgeneexpressionink562chronicmyelogenousleukemiccells
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