Vandetanib has antineoplastic activity in anaplastic thyroid cancer, in vitro and in vivo
The antitumor activity of vandetanib [a multiple signal transduction inhibitor including the RET tyrosine kinase, epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF) receptor (VEGFR), ERK and with antiangiogenic activity], in primary anaplastic thyroid cancer (ATC) cel...
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| Veröffentlicht in: | Oncology reports 2018-05, Vol.39 (5), p.2306-2314 |
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| creator | Ferrari, Silvia Martina Bocci, Guido Di Desidero, Teresa Ruffilli, Ilaria Elia, Giusy Ragusa, Francesca Fioravanti, Anna Orlandi, Paola Paparo, Sabrina Rosaria Patrizio, Armando Piaggi, Simona La Motta, Concettina Ulisse, Salvatore Baldini, Enke Materazzi, Gabriele Miccoli, Paolo Antonelli, Alessandro Fallahi, Poupak |
| description | The antitumor activity of vandetanib [a multiple signal transduction inhibitor including the RET tyrosine kinase, epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF) receptor (VEGFR), ERK and with antiangiogenic activity], in primary anaplastic thyroid cancer (ATC) cells, in the human cell line 8305C [undifferentiated thyroid cancer (TC)] and in an ATC‑cell line (AF), was investigated in the present study. Vandetanib (1 and 100 nM; 1, 10, 25 and 50 µM) was tested by WST‑1, apoptosis, migration and invasion assays: in primary ATC cells, in the 8305C continuous cell line, and in AF cells; and in 8305C cells in CD nu/nu mice. Vandetanib significantly reduced ATC cell proliferation (P |
| doi_str_mv | 10.3892/or.2018.6305 |
| format | Article |
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Vandetanib (1 and 100 nM; 1, 10, 25 and 50 µM) was tested by WST‑1, apoptosis, migration and invasion assays: in primary ATC cells, in the 8305C continuous cell line, and in AF cells; and in 8305C cells in CD nu/nu mice. Vandetanib significantly reduced ATC cell proliferation (P<0.01, ANOVA), induced apoptosis dose‑dependently (P<0.001, ANOVA), and inhibited migration (P<0.01) and invasion (P<0.001). Furthermore, vandetanib inhibited EGFR, AKT and ERK1/2 phosphorylation and downregulated cyclin D1 in ATC cells. In 8305C and AF cells, vandetanib significantly inhibited the proliferation, inducing also apoptosis. 8305C cells were injected subcutaneously in CD nu/nu mice and tumor masses became detectable after 30 days. Vandetanib (25 mg/kg/day) significantly inhibited tumor growth and VEGF‑A expression and microvessel density in 8305C tumor tissues. In conclusion, the antitumor and antiangiogenic activity of vandetanib is very auspicious in ATC, opening the way to a future clinical evaluation.</description><identifier>ISSN: 1021-335X</identifier><identifier>EISSN: 1791-2431</identifier><identifier>DOI: 10.3892/or.2018.6305</identifier><identifier>PMID: 29517106</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Animals ; Antineoplastic Agents - administration & dosage ; Antineoplastic Agents - pharmacology ; Apoptosis ; Cancer therapies ; Cell culture ; Cell cycle ; Cell growth ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cell Survival - drug effects ; Cyclin D1 - metabolism ; Deoxyribonucleic acid ; Development and progression ; DNA ; Dose-Response Relationship, Drug ; Drug therapy ; ErbB Receptors - metabolism ; FDA approval ; Gene Expression Regulation, Neoplastic - drug effects ; Growth factors ; Humans ; In Vitro Techniques ; Kinases ; Mice ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Mutation ; Patient outcomes ; Patients ; Penicillin ; Phosphorylation ; Piperidines - administration & dosage ; Piperidines - pharmacology ; Proto-Oncogene Proteins c-akt - metabolism ; Quinazolines - administration & dosage ; Quinazolines - pharmacology ; Studies ; Thyroid cancer ; Thyroid Carcinoma, Anaplastic - drug therapy ; Thyroid Carcinoma, Anaplastic - metabolism ; Thyroid Neoplasms - drug therapy ; Thyroid Neoplasms - metabolism ; Treatment Outcome ; Vandetanib ; Xenograft Model Antitumor Assays</subject><ispartof>Oncology reports, 2018-05, Vol.39 (5), p.2306-2314</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-e3e07c3a52488a1f8dbb6493cfafd93b77345358b88abd9bcc79d01852468e683</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27926,27927</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29517106$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ferrari, Silvia Martina</creatorcontrib><creatorcontrib>Bocci, Guido</creatorcontrib><creatorcontrib>Di Desidero, Teresa</creatorcontrib><creatorcontrib>Ruffilli, Ilaria</creatorcontrib><creatorcontrib>Elia, Giusy</creatorcontrib><creatorcontrib>Ragusa, Francesca</creatorcontrib><creatorcontrib>Fioravanti, Anna</creatorcontrib><creatorcontrib>Orlandi, Paola</creatorcontrib><creatorcontrib>Paparo, Sabrina Rosaria</creatorcontrib><creatorcontrib>Patrizio, Armando</creatorcontrib><creatorcontrib>Piaggi, Simona</creatorcontrib><creatorcontrib>La Motta, Concettina</creatorcontrib><creatorcontrib>Ulisse, Salvatore</creatorcontrib><creatorcontrib>Baldini, Enke</creatorcontrib><creatorcontrib>Materazzi, Gabriele</creatorcontrib><creatorcontrib>Miccoli, Paolo</creatorcontrib><creatorcontrib>Antonelli, Alessandro</creatorcontrib><creatorcontrib>Fallahi, Poupak</creatorcontrib><title>Vandetanib has antineoplastic activity in anaplastic thyroid cancer, in vitro and in vivo</title><title>Oncology reports</title><addtitle>Oncol Rep</addtitle><description>The antitumor activity of vandetanib [a multiple signal transduction inhibitor including the RET tyrosine kinase, epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF) receptor (VEGFR), ERK and with antiangiogenic activity], in primary anaplastic thyroid cancer (ATC) cells, in the human cell line 8305C [undifferentiated thyroid cancer (TC)] and in an ATC‑cell line (AF), was investigated in the present study. Vandetanib (1 and 100 nM; 1, 10, 25 and 50 µM) was tested by WST‑1, apoptosis, migration and invasion assays: in primary ATC cells, in the 8305C continuous cell line, and in AF cells; and in 8305C cells in CD nu/nu mice. Vandetanib significantly reduced ATC cell proliferation (P<0.01, ANOVA), induced apoptosis dose‑dependently (P<0.001, ANOVA), and inhibited migration (P<0.01) and invasion (P<0.001). Furthermore, vandetanib inhibited EGFR, AKT and ERK1/2 phosphorylation and downregulated cyclin D1 in ATC cells. In 8305C and AF cells, vandetanib significantly inhibited the proliferation, inducing also apoptosis. 8305C cells were injected subcutaneously in CD nu/nu mice and tumor masses became detectable after 30 days. Vandetanib (25 mg/kg/day) significantly inhibited tumor growth and VEGF‑A expression and microvessel density in 8305C tumor tissues. In conclusion, the antitumor and antiangiogenic activity of vandetanib is very auspicious in ATC, opening the way to a future clinical evaluation.</description><subject>Animals</subject><subject>Antineoplastic Agents - administration & dosage</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Cancer therapies</subject><subject>Cell culture</subject><subject>Cell cycle</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cell Survival - drug effects</subject><subject>Cyclin D1 - metabolism</subject><subject>Deoxyribonucleic acid</subject><subject>Development and progression</subject><subject>DNA</subject><subject>Dose-Response Relationship, Drug</subject><subject>Drug therapy</subject><subject>ErbB Receptors - metabolism</subject><subject>FDA approval</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Growth factors</subject><subject>Humans</subject><subject>In Vitro Techniques</subject><subject>Kinases</subject><subject>Mice</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Mutation</subject><subject>Patient outcomes</subject><subject>Patients</subject><subject>Penicillin</subject><subject>Phosphorylation</subject><subject>Piperidines - administration & dosage</subject><subject>Piperidines - pharmacology</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Quinazolines - administration & dosage</subject><subject>Quinazolines - pharmacology</subject><subject>Studies</subject><subject>Thyroid cancer</subject><subject>Thyroid Carcinoma, Anaplastic - drug therapy</subject><subject>Thyroid Carcinoma, Anaplastic - metabolism</subject><subject>Thyroid Neoplasms - drug therapy</subject><subject>Thyroid Neoplasms - metabolism</subject><subject>Treatment Outcome</subject><subject>Vandetanib</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1021-335X</issn><issn>1791-2431</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkUtLAzEUhYMovneuZUBw5dQ8Jo9ZivgCwY2KrkImydjINKlJKvTfm9LWB0gWyb3nuzccDgBHCI6IaPF5iCMMkRgxAukG2EW8RTVuCNosb4hRTQh92QF7Kb1DiDlk7TbYwS1FHEG2C16flTc2K--6aqxSpXx23obpoFJ2ulI6u0-X55XzRVLrdh7PY3Cm0sprG88WaqFiKIxZFp_hAGz1akj2cHXvg6frq8fL2_r-4ebu8uK-1g2lubbEQq6JorgRQqFemK5jTUt0r3rTko5z0lBCRVfUzrSd1rw1xW_hmbBMkH1wstw7jeFjZlOW72EWfflS4uKfccZo80O9qcFK5_uQo9ITl7S8KOsbjATHhRr9Q5Vj7MTp4G3vSv_PwOmvgbFVQx6nMMyyCz79Bc-WoI4hpWh7OY1uouJcIigXOcoQ5SJHucix4McrU7NuYs03vA6OfAE_hZY2</recordid><startdate>20180501</startdate><enddate>20180501</enddate><creator>Ferrari, Silvia Martina</creator><creator>Bocci, Guido</creator><creator>Di Desidero, Teresa</creator><creator>Ruffilli, Ilaria</creator><creator>Elia, Giusy</creator><creator>Ragusa, Francesca</creator><creator>Fioravanti, Anna</creator><creator>Orlandi, Paola</creator><creator>Paparo, Sabrina Rosaria</creator><creator>Patrizio, Armando</creator><creator>Piaggi, Simona</creator><creator>La Motta, Concettina</creator><creator>Ulisse, Salvatore</creator><creator>Baldini, Enke</creator><creator>Materazzi, Gabriele</creator><creator>Miccoli, Paolo</creator><creator>Antonelli, Alessandro</creator><creator>Fallahi, Poupak</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope></search><sort><creationdate>20180501</creationdate><title>Vandetanib has antineoplastic activity in anaplastic thyroid cancer, in vitro and in vivo</title><author>Ferrari, Silvia Martina ; Bocci, Guido ; Di Desidero, Teresa ; Ruffilli, Ilaria ; Elia, Giusy ; Ragusa, Francesca ; Fioravanti, Anna ; Orlandi, Paola ; Paparo, Sabrina Rosaria ; Patrizio, Armando ; Piaggi, Simona ; La Motta, Concettina ; Ulisse, Salvatore ; Baldini, Enke ; Materazzi, Gabriele ; Miccoli, Paolo ; Antonelli, Alessandro ; Fallahi, Poupak</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-e3e07c3a52488a1f8dbb6493cfafd93b77345358b88abd9bcc79d01852468e683</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Antineoplastic Agents - administration & dosage</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Cancer therapies</topic><topic>Cell culture</topic><topic>Cell cycle</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cell Survival - drug effects</topic><topic>Cyclin D1 - metabolism</topic><topic>Deoxyribonucleic acid</topic><topic>Development and progression</topic><topic>DNA</topic><topic>Dose-Response Relationship, Drug</topic><topic>Drug therapy</topic><topic>ErbB Receptors - metabolism</topic><topic>FDA approval</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Growth factors</topic><topic>Humans</topic><topic>In Vitro Techniques</topic><topic>Kinases</topic><topic>Mice</topic><topic>Mitogen-Activated Protein Kinase 1 - metabolism</topic><topic>Mitogen-Activated Protein Kinase 3 - metabolism</topic><topic>Mutation</topic><topic>Patient outcomes</topic><topic>Patients</topic><topic>Penicillin</topic><topic>Phosphorylation</topic><topic>Piperidines - 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Vandetanib (1 and 100 nM; 1, 10, 25 and 50 µM) was tested by WST‑1, apoptosis, migration and invasion assays: in primary ATC cells, in the 8305C continuous cell line, and in AF cells; and in 8305C cells in CD nu/nu mice. Vandetanib significantly reduced ATC cell proliferation (P<0.01, ANOVA), induced apoptosis dose‑dependently (P<0.001, ANOVA), and inhibited migration (P<0.01) and invasion (P<0.001). Furthermore, vandetanib inhibited EGFR, AKT and ERK1/2 phosphorylation and downregulated cyclin D1 in ATC cells. In 8305C and AF cells, vandetanib significantly inhibited the proliferation, inducing also apoptosis. 8305C cells were injected subcutaneously in CD nu/nu mice and tumor masses became detectable after 30 days. Vandetanib (25 mg/kg/day) significantly inhibited tumor growth and VEGF‑A expression and microvessel density in 8305C tumor tissues. In conclusion, the antitumor and antiangiogenic activity of vandetanib is very auspicious in ATC, opening the way to a future clinical evaluation.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29517106</pmid><doi>10.3892/or.2018.6305</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Oncology reports, 2018-05, Vol.39 (5), p.2306-2314 |
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| source | MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Antineoplastic Agents - administration & dosage Antineoplastic Agents - pharmacology Apoptosis Cancer therapies Cell culture Cell cycle Cell growth Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Cyclin D1 - metabolism Deoxyribonucleic acid Development and progression DNA Dose-Response Relationship, Drug Drug therapy ErbB Receptors - metabolism FDA approval Gene Expression Regulation, Neoplastic - drug effects Growth factors Humans In Vitro Techniques Kinases Mice Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Mutation Patient outcomes Patients Penicillin Phosphorylation Piperidines - administration & dosage Piperidines - pharmacology Proto-Oncogene Proteins c-akt - metabolism Quinazolines - administration & dosage Quinazolines - pharmacology Studies Thyroid cancer Thyroid Carcinoma, Anaplastic - drug therapy Thyroid Carcinoma, Anaplastic - metabolism Thyroid Neoplasms - drug therapy Thyroid Neoplasms - metabolism Treatment Outcome Vandetanib Xenograft Model Antitumor Assays |
| title | Vandetanib has antineoplastic activity in anaplastic thyroid cancer, in vitro and in vivo |
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