Up-regulation of HER2 by gemcitabine enhances the antitumor effect of combined gemcitabine and trastuzumab emtansine treatment on pancreatic ductal adenocarcinoma cells
Although pancreatic ductal adenocarcinomas (PDAs) widely express HER2, the expression level is generally low. If HER2 expression in PDA cells could be enhanced by treatment with a given agent, then combination therapy with that agent and trastuzumab emtansine (T-DM1), a chemotherapeutic agent that i...
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| Veröffentlicht in: | BMC cancer 2015-10, Vol.15 (1), p.726-726, Article 726 |
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| creator | Kan, Shin Koido, Shigeo Okamoto, Masato Hayashi, Kazumi Ito, Masaki Kamata, Yuko Komita, Hideo Nagasaki, Eijiro Homma, Sadamu |
| description | Although pancreatic ductal adenocarcinomas (PDAs) widely express HER2, the expression level is generally low. If HER2 expression in PDA cells could be enhanced by treatment with a given agent, then combination therapy with that agent and trastuzumab emtansine (T-DM1), a chemotherapeutic agent that is a conjugate of trastuzumab, might lead to significant antitumor effects against PDA.
Cell proliferation was examined by spectrophotometry. HER2 expression was examined by flow cytometry, immunoblot and quantitative reverse transcription polymerase chain reaction. T-DM1 binding to cells was examined by flow cytometry and enzyme-linked immunosorbent assay.
Out of 5 tested human PDA cell lines, including MIA PaCa-2, three showed increases in HER2 expression after gemcitabine (GEM) treatment. The binding of T-DM1 to GEM-treated MIA PaCa-2 cells was higher than to untreated MIA PaCa-2 cells. Treatment with GEM and T-DM1 showed synergic cytotoxic effects on MIA PaCa-2 cells in vitro. Cells in the G2M phase of the cell cycle were retained after GEM treatment and showed higher levels of HER2 expression, possibly contributing to the synergic effect of GEM and T-DM1.
Combined treatment with GEM and T-DM1 might confer a potent therapeutic modality against PDA as a result of GEM-mediated HER2 up-regulation. |
| doi_str_mv | 10.1186/s12885-015-1772-1 |
| format | Article |
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Cell proliferation was examined by spectrophotometry. HER2 expression was examined by flow cytometry, immunoblot and quantitative reverse transcription polymerase chain reaction. T-DM1 binding to cells was examined by flow cytometry and enzyme-linked immunosorbent assay.
Out of 5 tested human PDA cell lines, including MIA PaCa-2, three showed increases in HER2 expression after gemcitabine (GEM) treatment. The binding of T-DM1 to GEM-treated MIA PaCa-2 cells was higher than to untreated MIA PaCa-2 cells. Treatment with GEM and T-DM1 showed synergic cytotoxic effects on MIA PaCa-2 cells in vitro. Cells in the G2M phase of the cell cycle were retained after GEM treatment and showed higher levels of HER2 expression, possibly contributing to the synergic effect of GEM and T-DM1.
Combined treatment with GEM and T-DM1 might confer a potent therapeutic modality against PDA as a result of GEM-mediated HER2 up-regulation.</description><identifier>ISSN: 1471-2407</identifier><identifier>EISSN: 1471-2407</identifier><identifier>DOI: 10.1186/s12885-015-1772-1</identifier><identifier>PMID: 26475267</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject><![CDATA[Adenocarcinoma ; Adenocarcinoma - drug therapy ; Adenocarcinoma - genetics ; Adenocarcinoma - pathology ; Animals ; Antibodies ; Antibodies, Monoclonal, Humanized - administration & dosage ; Antineoplastic Combined Chemotherapy Protocols - administration & dosage ; Breast cancer ; Cancer ; Cancer therapies ; Care and treatment ; Cell cycle ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Chemotherapy ; Complications and side effects ; Cytotoxicity ; Deoxycytidine - administration & dosage ; Deoxycytidine - analogs & derivatives ; Drug therapy ; Epidermal growth factor ; Gastric cancer ; Gene amplification ; Gene Expression Regulation, Neoplastic - drug effects ; Health aspects ; Humans ; Kinases ; Maytansine - administration & dosage ; Maytansine - analogs & derivatives ; Medical prognosis ; Metastasis ; Mice ; Pancreatic cancer ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - pathology ; Proteins ; Receptor, ErbB-2 - biosynthesis ; Receptor, ErbB-2 - genetics ; Signal transduction ; Trastuzumab ; Xenograft Model Antitumor Assays]]></subject><ispartof>BMC cancer, 2015-10, Vol.15 (1), p.726-726, Article 726</ispartof><rights>COPYRIGHT 2015 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2015</rights><rights>Kan et al. 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c625t-f5c14880030676cd031072e1a599de164fd994e8009d842cfa14e17b8941b6963</citedby><cites>FETCH-LOGICAL-c625t-f5c14880030676cd031072e1a599de164fd994e8009d842cfa14e17b8941b6963</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609140/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4609140/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26475267$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kan, Shin</creatorcontrib><creatorcontrib>Koido, Shigeo</creatorcontrib><creatorcontrib>Okamoto, Masato</creatorcontrib><creatorcontrib>Hayashi, Kazumi</creatorcontrib><creatorcontrib>Ito, Masaki</creatorcontrib><creatorcontrib>Kamata, Yuko</creatorcontrib><creatorcontrib>Komita, Hideo</creatorcontrib><creatorcontrib>Nagasaki, Eijiro</creatorcontrib><creatorcontrib>Homma, Sadamu</creatorcontrib><title>Up-regulation of HER2 by gemcitabine enhances the antitumor effect of combined gemcitabine and trastuzumab emtansine treatment on pancreatic ductal adenocarcinoma cells</title><title>BMC cancer</title><addtitle>BMC Cancer</addtitle><description>Although pancreatic ductal adenocarcinomas (PDAs) widely express HER2, the expression level is generally low. If HER2 expression in PDA cells could be enhanced by treatment with a given agent, then combination therapy with that agent and trastuzumab emtansine (T-DM1), a chemotherapeutic agent that is a conjugate of trastuzumab, might lead to significant antitumor effects against PDA.
Cell proliferation was examined by spectrophotometry. HER2 expression was examined by flow cytometry, immunoblot and quantitative reverse transcription polymerase chain reaction. T-DM1 binding to cells was examined by flow cytometry and enzyme-linked immunosorbent assay.
Out of 5 tested human PDA cell lines, including MIA PaCa-2, three showed increases in HER2 expression after gemcitabine (GEM) treatment. The binding of T-DM1 to GEM-treated MIA PaCa-2 cells was higher than to untreated MIA PaCa-2 cells. Treatment with GEM and T-DM1 showed synergic cytotoxic effects on MIA PaCa-2 cells in vitro. Cells in the G2M phase of the cell cycle were retained after GEM treatment and showed higher levels of HER2 expression, possibly contributing to the synergic effect of GEM and T-DM1.
Combined treatment with GEM and T-DM1 might confer a potent therapeutic modality against PDA as a result of GEM-mediated HER2 up-regulation.</description><subject>Adenocarcinoma</subject><subject>Adenocarcinoma - drug therapy</subject><subject>Adenocarcinoma - genetics</subject><subject>Adenocarcinoma - pathology</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antibodies, Monoclonal, Humanized - administration & dosage</subject><subject>Antineoplastic Combined Chemotherapy Protocols - administration & dosage</subject><subject>Breast cancer</subject><subject>Cancer</subject><subject>Cancer therapies</subject><subject>Care and treatment</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Chemotherapy</subject><subject>Complications and side effects</subject><subject>Cytotoxicity</subject><subject>Deoxycytidine - administration & dosage</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Drug therapy</subject><subject>Epidermal growth factor</subject><subject>Gastric cancer</subject><subject>Gene amplification</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Kinases</subject><subject>Maytansine - administration & dosage</subject><subject>Maytansine - analogs & derivatives</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Pancreatic cancer</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Proteins</subject><subject>Receptor, ErbB-2 - biosynthesis</subject><subject>Receptor, ErbB-2 - genetics</subject><subject>Signal transduction</subject><subject>Trastuzumab</subject><subject>Xenograft Model Antitumor Assays</subject><issn>1471-2407</issn><issn>1471-2407</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkl9r1TAYxosobk4_gDcSEEQvOvOmadLeCGNMNxgI012HNH17TkabHJNUnJ_Ij2nK5jwVyUX-_Z4neZOnKF4CPQZoxPsIrGnqkkJdgpSshEfFIXAJJeNUPt4bHxTPYryhFGRDm6fFARNc1kzIw-LX9a4MuJlHnax3xA_k_OyKke6WbHAyNunOOiTottoZjCRtkWiXbJonHwgOA5q0iIyfFrBfqbTrSQo6pvnnPOmO4JS0i8tOCqjThC5rHdll62VuDelnk_RIdI_OGx2MdX7SxOA4xufFk0GPEV_c90fF9cezr6fn5eXnTxenJ5elEaxO5VAb4E1DaUWFFKanFVDJEHTdtj2C4EPfthwz0PYNZ2bQwBFk17QcOtGK6qj4cOe7m7sJe5MvGfSodsFOOtwqr61a7zi7VRv_XXFBW-A0G7y9Nwj-24wxqcnGpQTt0M9RgWScCVpVMqOv_0Fv_BxcLi9Tsm1Y_qP6L7XRIyrrBp_PNYupOql5PpJxWO59_B8qtx4na7zDweb1leDdSpCZhD_SRs8xqosvV2v2zR67RT2mbfTjvGQmrkG4A03wMQYcHh4OqFoyq-4yq3JmlxqZgqx5tf_iD4o_Ia1-A5_p5zs</recordid><startdate>20151016</startdate><enddate>20151016</enddate><creator>Kan, Shin</creator><creator>Koido, Shigeo</creator><creator>Okamoto, Masato</creator><creator>Hayashi, Kazumi</creator><creator>Ito, Masaki</creator><creator>Kamata, Yuko</creator><creator>Komita, Hideo</creator><creator>Nagasaki, Eijiro</creator><creator>Homma, Sadamu</creator><general>BioMed Central Ltd</general><general>BioMed Central</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>ISR</scope><scope>3V.</scope><scope>7TO</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>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20151016</creationdate><title>Up-regulation of HER2 by gemcitabine enhances the antitumor effect of combined gemcitabine and trastuzumab emtansine treatment on pancreatic ductal adenocarcinoma cells</title><author>Kan, Shin ; Koido, Shigeo ; Okamoto, Masato ; Hayashi, Kazumi ; Ito, Masaki ; Kamata, Yuko ; Komita, Hideo ; Nagasaki, Eijiro ; Homma, Sadamu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c625t-f5c14880030676cd031072e1a599de164fd994e8009d842cfa14e17b8941b6963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adenocarcinoma</topic><topic>Adenocarcinoma - drug therapy</topic><topic>Adenocarcinoma - genetics</topic><topic>Adenocarcinoma - pathology</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antibodies, Monoclonal, Humanized - administration & dosage</topic><topic>Antineoplastic Combined Chemotherapy Protocols - administration & dosage</topic><topic>Breast cancer</topic><topic>Cancer</topic><topic>Cancer therapies</topic><topic>Care and treatment</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Chemotherapy</topic><topic>Complications and side effects</topic><topic>Cytotoxicity</topic><topic>Deoxycytidine - administration & dosage</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Drug therapy</topic><topic>Epidermal growth factor</topic><topic>Gastric cancer</topic><topic>Gene amplification</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Kinases</topic><topic>Maytansine - administration & dosage</topic><topic>Maytansine - analogs & derivatives</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Mice</topic><topic>Pancreatic cancer</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Proteins</topic><topic>Receptor, ErbB-2 - biosynthesis</topic><topic>Receptor, ErbB-2 - genetics</topic><topic>Signal transduction</topic><topic>Trastuzumab</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kan, Shin</creatorcontrib><creatorcontrib>Koido, Shigeo</creatorcontrib><creatorcontrib>Okamoto, Masato</creatorcontrib><creatorcontrib>Hayashi, Kazumi</creatorcontrib><creatorcontrib>Ito, Masaki</creatorcontrib><creatorcontrib>Kamata, Yuko</creatorcontrib><creatorcontrib>Komita, Hideo</creatorcontrib><creatorcontrib>Nagasaki, Eijiro</creatorcontrib><creatorcontrib>Homma, Sadamu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC cancer</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kan, Shin</au><au>Koido, Shigeo</au><au>Okamoto, Masato</au><au>Hayashi, Kazumi</au><au>Ito, Masaki</au><au>Kamata, Yuko</au><au>Komita, Hideo</au><au>Nagasaki, Eijiro</au><au>Homma, Sadamu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Up-regulation of HER2 by gemcitabine enhances the antitumor effect of combined gemcitabine and trastuzumab emtansine treatment on pancreatic ductal adenocarcinoma cells</atitle><jtitle>BMC cancer</jtitle><addtitle>BMC Cancer</addtitle><date>2015-10-16</date><risdate>2015</risdate><volume>15</volume><issue>1</issue><spage>726</spage><epage>726</epage><pages>726-726</pages><artnum>726</artnum><issn>1471-2407</issn><eissn>1471-2407</eissn><abstract>Although pancreatic ductal adenocarcinomas (PDAs) widely express HER2, the expression level is generally low. If HER2 expression in PDA cells could be enhanced by treatment with a given agent, then combination therapy with that agent and trastuzumab emtansine (T-DM1), a chemotherapeutic agent that is a conjugate of trastuzumab, might lead to significant antitumor effects against PDA.
Cell proliferation was examined by spectrophotometry. HER2 expression was examined by flow cytometry, immunoblot and quantitative reverse transcription polymerase chain reaction. T-DM1 binding to cells was examined by flow cytometry and enzyme-linked immunosorbent assay.
Out of 5 tested human PDA cell lines, including MIA PaCa-2, three showed increases in HER2 expression after gemcitabine (GEM) treatment. The binding of T-DM1 to GEM-treated MIA PaCa-2 cells was higher than to untreated MIA PaCa-2 cells. Treatment with GEM and T-DM1 showed synergic cytotoxic effects on MIA PaCa-2 cells in vitro. Cells in the G2M phase of the cell cycle were retained after GEM treatment and showed higher levels of HER2 expression, possibly contributing to the synergic effect of GEM and T-DM1.
Combined treatment with GEM and T-DM1 might confer a potent therapeutic modality against PDA as a result of GEM-mediated HER2 up-regulation.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26475267</pmid><doi>10.1186/s12885-015-1772-1</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenocarcinoma Adenocarcinoma - drug therapy Adenocarcinoma - genetics Adenocarcinoma - pathology Animals Antibodies Antibodies, Monoclonal, Humanized - administration & dosage Antineoplastic Combined Chemotherapy Protocols - administration & dosage Breast cancer Cancer Cancer therapies Care and treatment Cell cycle Cell Line, Tumor Cell Proliferation - drug effects Chemotherapy Complications and side effects Cytotoxicity Deoxycytidine - administration & dosage Deoxycytidine - analogs & derivatives Drug therapy Epidermal growth factor Gastric cancer Gene amplification Gene Expression Regulation, Neoplastic - drug effects Health aspects Humans Kinases Maytansine - administration & dosage Maytansine - analogs & derivatives Medical prognosis Metastasis Mice Pancreatic cancer Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - pathology Proteins Receptor, ErbB-2 - biosynthesis Receptor, ErbB-2 - genetics Signal transduction Trastuzumab Xenograft Model Antitumor Assays |
| title | Up-regulation of HER2 by gemcitabine enhances the antitumor effect of combined gemcitabine and trastuzumab emtansine treatment on pancreatic ductal adenocarcinoma cells |
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