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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Modulation of the insulin-like growth factor-I system by N-(4-hydroxyphenyl)-retinamide in human breast cancer cell lines.</title><author><name sortKey="Favoni, R E" sort="Favoni, R E" uniqKey="Favoni R" first="R. E." last="Favoni">R. E. Favoni</name></author><author><name sortKey="De Cupis, A" sort="De Cupis, A" uniqKey="De Cupis A" first="A." last="De Cupis">A. De Cupis</name></author><author><name sortKey="Bruno, S" sort="Bruno, S" uniqKey="Bruno S" first="S." last="Bruno">S. Bruno</name></author><author><name sortKey="Yee, D" sort="Yee, D" uniqKey="Yee D" first="D." last="Yee">D. Yee</name></author><author><name sortKey="Ferrera, A" sort="Ferrera, A" uniqKey="Ferrera A" first="A." last="Ferrera">A. Ferrera</name></author><author><name sortKey="Pirani, P" sort="Pirani, P" uniqKey="Pirani P" first="P." last="Pirani">P. Pirani</name></author><author><name sortKey="Costa, A" sort="Costa, A" uniqKey="Costa A" first="A." last="Costa">A. Costa</name></author><author><name sortKey="Decensi, A" sort="Decensi, A" uniqKey="Decensi A" first="A." last="Decensi">A. Decensi</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">9649125</idno><idno type="pmc">2150424</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2150424</idno><idno type="RBID">PMC:2150424</idno><date when="1998">1998</date><idno type="wicri:Area/Pmc/Corpus">000180</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000180</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Modulation of the insulin-like growth factor-I system by N-(4-hydroxyphenyl)-retinamide in human breast cancer cell lines.</title><author><name sortKey="Favoni, R E" sort="Favoni, R E" uniqKey="Favoni R" first="R. E." last="Favoni">R. E. Favoni</name></author><author><name sortKey="De Cupis, A" sort="De Cupis, A" uniqKey="De Cupis A" first="A." last="De Cupis">A. De Cupis</name></author><author><name sortKey="Bruno, S" sort="Bruno, S" uniqKey="Bruno S" first="S." last="Bruno">S. Bruno</name></author><author><name sortKey="Yee, D" sort="Yee, D" uniqKey="Yee D" first="D." last="Yee">D. Yee</name></author><author><name sortKey="Ferrera, A" sort="Ferrera, A" uniqKey="Ferrera A" first="A." last="Ferrera">A. Ferrera</name></author><author><name sortKey="Pirani, P" sort="Pirani, P" uniqKey="Pirani P" first="P." last="Pirani">P. Pirani</name></author><author><name sortKey="Costa, A" sort="Costa, A" uniqKey="Costa A" first="A." last="Costa">A. Costa</name></author><author><name sortKey="Decensi, A" sort="Decensi, A" uniqKey="Decensi A" first="A." last="Decensi">A. Decensi</name></author></analytic><series><title level="j">British Journal of Cancer</title><idno type="ISSN">0007-0920</idno><idno type="eISSN">1532-1827</idno><imprint><date when="1998">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>The potent mitogenic activity of insulin-like growth factor I (IGF-I) on breast epithelium is inhibited by retinoic acid in oestrogen receptor-positive (ER+) breast cancer cell lines. We studied and compared the effects of N-(4-hydroxyphenyl)-retinamide (4-HPR) in terms of growth inhibition and modulation of the IGF-I system in ER+ (MCF-7) and oestrogen receptor-negative (ER-) (MDA-MB231) breast cancer cell lines. Treatment with 1-10 microM 4-HPR for up to 96 h induced a dose- and time-dependent inhibition of proliferation in both breast cancer cell lines. Induction of apoptosis was much more evident in MCF-7 than in MDA-MB231 cells (30-40% compared with 0-5% respectively at 5 microM for 48 h). Exogenous human recombinant IGF-I (hr-IGF-I)-stimulated cell proliferation was abolished by 1 microM 4-HPR in MCF-7 cells. Immunoreactive IGF-I-like protein concentration in conditioned medium was reduced by 38% in MCF-7 and by 90% in MDA-MB231 cell lines following treatment for 48 h with 5 microM 4-HPR. Western ligand blot analysis showed a reduction of IGF-binding protein 4 (BP4) and BP5 by 67% and 87%, respectively, in MCF-7, whereas IGF-BP4 and -BP1 were reduced by approximately 20% in MDA-MB231 cells. Exposure to 5 microM 4-HPR for 48 h inhibited [125I]IGF-I binding and Scatchard analysis revealed a decrease of more than 50% in maximum binding capacity (Bmax) and a reduced receptor number/cell in both cancer cell lines. Steady-state type I IGF-receptor mRNA levels were reduced by approximately 30% in both tumour cell lines. We conclude that 4-HPR induces a significant down-regulation of the IGF-I system in both ER+ (MCF-7) and ER- (MDA-MB231) breast cancer cell lines. These findings suggest that, in our model, interference with the ER signalling pathway is not the only mechanism of breast cancer growth inhibition by 4-HPR.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Figure 6</label><graphic xlink:href="brjcancer00088-0089-a" xlink:role="2143"></graphic></fig><fig id="F2"><label>Figure 8</label><graphic xlink:href="brjcancer00088-0091-a" xlink:role="2145"></graphic></fig></sec></div></front></TEI><pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Br J Cancer</journal-id><journal-id journal-id-type="pmc">brjcancer</journal-id><journal-title>British Journal of Cancer</journal-title><issn pub-type="ppub">0007-0920</issn><issn pub-type="epub">1532-1827</issn><publisher><publisher-name>Nature Publishing Group</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">9649125</article-id><article-id pub-id-type="pmc">2150424</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group></article-categories><title-group><article-title>Modulation of the insulin-like growth factor-I system by N-(4-hydroxyphenyl)-retinamide in human breast cancer cell lines.</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Favoni</surname><given-names>R. E.</given-names></name></contrib><contrib contrib-type="author"><name><surname>de Cupis</surname><given-names>A.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Bruno</surname><given-names>S.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Yee</surname><given-names>D.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Ferrera</surname><given-names>A.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Pirani</surname><given-names>P.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Costa</surname><given-names>A.</given-names></name></contrib><contrib contrib-type="author"><name><surname>Decensi</surname><given-names>A.</given-names></name></contrib></contrib-group><aff>Department of Preclinical Oncology, National Institute for Cancer Research and Advanced Biotechnology Center, Genoa, Italy.</aff><pub-date pub-type="ppub"><month>6</month><year>1998</year></pub-date><volume>77</volume><issue>12</issue><fpage>2138</fpage><lpage>2147</lpage><abstract><p>The potent mitogenic activity of insulin-like growth factor I (IGF-I) on breast epithelium is inhibited by retinoic acid in oestrogen receptor-positive (ER+) breast cancer cell lines. We studied and compared the effects of N-(4-hydroxyphenyl)-retinamide (4-HPR) in terms of growth inhibition and modulation of the IGF-I system in ER+ (MCF-7) and oestrogen receptor-negative (ER-) (MDA-MB231) breast cancer cell lines. Treatment with 1-10 microM 4-HPR for up to 96 h induced a dose- and time-dependent inhibition of proliferation in both breast cancer cell lines. Induction of apoptosis was much more evident in MCF-7 than in MDA-MB231 cells (30-40% compared with 0-5% respectively at 5 microM for 48 h). Exogenous human recombinant IGF-I (hr-IGF-I)-stimulated cell proliferation was abolished by 1 microM 4-HPR in MCF-7 cells. Immunoreactive IGF-I-like protein concentration in conditioned medium was reduced by 38% in MCF-7 and by 90% in MDA-MB231 cell lines following treatment for 48 h with 5 microM 4-HPR. Western ligand blot analysis showed a reduction of IGF-binding protein 4 (BP4) and BP5 by 67% and 87%, respectively, in MCF-7, whereas IGF-BP4 and -BP1 were reduced by approximately 20% in MDA-MB231 cells. Exposure to 5 microM 4-HPR for 48 h inhibited [125I]IGF-I binding and Scatchard analysis revealed a decrease of more than 50% in maximum binding capacity (Bmax) and a reduced receptor number/cell in both cancer cell lines. Steady-state type I IGF-receptor mRNA levels were reduced by approximately 30% in both tumour cell lines. We conclude that 4-HPR induces a significant down-regulation of the IGF-I system in both ER+ (MCF-7) and ER- (MDA-MB231) breast cancer cell lines. These findings suggest that, in our model, interference with the ER signalling pathway is not the only mechanism of breast cancer growth inhibition by 4-HPR.</p><sec sec-type="scanned-figures"><title>Images</title><fig id="F1"><label>Figure 6</label><graphic xlink:href="brjcancer00088-0089-a" xlink:role="2143"></graphic></fig><fig id="F2"><label>Figure 8</label><graphic xlink:href="brjcancer00088-0091-a" xlink:role="2145"></graphic></fig></sec></abstract></article-meta></front><body><supplementary-material content-type="scanned-pages"><graphic xlink:href="brjcancer00088-0084.tif" xlink:title="scanned-page" xlink:role="2138" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0085.tif" xlink:title="scanned-page" xlink:role="2139" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0086.tif" xlink:title="scanned-page" xlink:role="2140" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0087.tif" xlink:title="scanned-page" xlink:role="2141" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0088.tif" xlink:title="scanned-page" xlink:role="2142" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0089.tif" xlink:title="scanned-page" xlink:role="2143" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0090.tif" xlink:title="scanned-page" xlink:role="2144" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0091.tif" xlink:title="scanned-page" xlink:role="2145" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0092.tif" xlink:title="scanned-page" xlink:role="2146" mimetype="image" mime-subtype="tiff"></graphic><graphic xlink:href="brjcancer00088-0093.tif" xlink:title="scanned-page" xlink:role="2147" mimetype="image" mime-subtype="tiff"></graphic></supplementary-material></body></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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