Extracelluar matrix metalloproteinase as a novel target for pancreatic cancer therapy
The objective of this study was to evaluate extracellular matrix metalloproteinase (EMMPRIN) as a novel target in orthotopic pancreatic cancer murine models. MIA PaCa-2 human pancreatic tumor cells were implanted in groups 1 and 3–7, whereas MIA PaCa-2 EMMPRIN knockdown cells were implanted in group...
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| Veröffentlicht in: | Anti-cancer drugs 2011-10, Vol.22 (9), p.864-874 |
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| creator | Kim, Hyunki Zhai, Guihua Liu, Zhiyong Samuel, Sharon Shah, Nemil Helman, Emily E Knowles, Joseph A Stockard, Cecil R Fineberg, Naomi S Grizzle, William E Zhou, Tong Zinn, Kurt R Rosenthal, Eben L |
| description | The objective of this study was to evaluate extracellular matrix metalloproteinase (EMMPRIN) as a novel target in orthotopic pancreatic cancer murine models. MIA PaCa-2 human pancreatic tumor cells were implanted in groups 1 and 3–7, whereas MIA PaCa-2 EMMPRIN knockdown cells were implanted in group 2. Dosing with anti-EMMPRIN antibody started immediately after implantation for groups 1–3 (residual tumor model) and at 21 days after cell implantation for groups 4–7 (established tumor model). Groups 3, 5, and 7 were treated with anti-EMMRPIN antibody (0.2–1.0 mg) twice weekly for 2–3 weeks, whereas the other groups served as the control. In the residual tumor model, tumor growth of anti-EMMPRIN-treated group was successfully arrested for 21 days (15±4 mm), which was significantly lower than that of the EMMPRIN knockdown group (80±15 mm; P=0.001) or the control group (240±41 mm; P |
| doi_str_mv | 10.1097/CAD.0b013e328349311e |
| format | Article |
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MIA PaCa-2 human pancreatic tumor cells were implanted in groups 1 and 3–7, whereas MIA PaCa-2 EMMPRIN knockdown cells were implanted in group 2. Dosing with anti-EMMPRIN antibody started immediately after implantation for groups 1–3 (residual tumor model) and at 21 days after cell implantation for groups 4–7 (established tumor model). Groups 3, 5, and 7 were treated with anti-EMMRPIN antibody (0.2–1.0 mg) twice weekly for 2–3 weeks, whereas the other groups served as the control. In the residual tumor model, tumor growth of anti-EMMPRIN-treated group was successfully arrested for 21 days (15±4 mm), which was significantly lower than that of the EMMPRIN knockdown group (80±15 mm; P=0.001) or the control group (240±41 mm; P<0.001). In the established tumor model, anti-EMMPRIN therapy lowered tumor volume increase by approximately 40% compared with the control, regardless of the dose amount. Ki67-expressed cell density of group 5 was 939±150 mm, which was significantly lower than that of group 4 (1709±145 mm; P=0.006). Microvessel density of group 5 (30±6 mm) was also significantly lower than that of group 4 (53±5 mm; P=0.014), whereas the microvessel size of group 5 (191±22 μm) was significantly larger than that of group 4 (113±26 μm; P=0.049). These data show the high potential of anti-EMMPRIN therapy for pancreatic cancer and support its clinical translation.</description><identifier>ISSN: 0959-4973</identifier><identifier>EISSN: 1473-5741</identifier><identifier>DOI: 10.1097/CAD.0b013e328349311e</identifier><identifier>PMID: 21730821</identifier><language>eng</language><publisher>England: Lippincott Williams & Wilkins, Inc</publisher><subject>Animals ; Antibodies, Anti-Idiotypic - immunology ; Antibodies, Anti-Idiotypic - pharmacology ; Antibodies, Monoclonal, Murine-Derived - immunology ; Antibodies, Monoclonal, Murine-Derived - therapeutic use ; Basigin - biosynthesis ; Basigin - immunology ; Basigin - metabolism ; Cell Line, Tumor ; Drug Evaluation, Preclinical ; Extracellular Matrix - metabolism ; Female ; Gene Knockdown Techniques ; Humans ; Ki-67 Antigen - biosynthesis ; Ki-67 Antigen - metabolism ; Matrix Metalloproteinases - metabolism ; Mice ; Mice, Inbred BALB C ; Mice, SCID ; Molecular Targeted Therapy ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - metabolism ; Pancreatic Neoplasms - pathology ; Radioimmunoassay ; Tumor Burden - drug effects ; Xenograft Model Antitumor Assays</subject><ispartof>Anti-cancer drugs, 2011-10, Vol.22 (9), p.864-874</ispartof><rights>2011 Lippincott Williams & Wilkins, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433e-bd0558e2639ee24c8ffbfdc3460508d4f608debb097a30889db501a80d1cdc003</citedby><cites>FETCH-LOGICAL-c433e-bd0558e2639ee24c8ffbfdc3460508d4f608debb097a30889db501a80d1cdc003</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21730821$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Hyunki</creatorcontrib><creatorcontrib>Zhai, Guihua</creatorcontrib><creatorcontrib>Liu, Zhiyong</creatorcontrib><creatorcontrib>Samuel, Sharon</creatorcontrib><creatorcontrib>Shah, Nemil</creatorcontrib><creatorcontrib>Helman, Emily E</creatorcontrib><creatorcontrib>Knowles, Joseph A</creatorcontrib><creatorcontrib>Stockard, Cecil R</creatorcontrib><creatorcontrib>Fineberg, Naomi S</creatorcontrib><creatorcontrib>Grizzle, William E</creatorcontrib><creatorcontrib>Zhou, Tong</creatorcontrib><creatorcontrib>Zinn, Kurt R</creatorcontrib><creatorcontrib>Rosenthal, Eben L</creatorcontrib><title>Extracelluar matrix metalloproteinase as a novel target for pancreatic cancer therapy</title><title>Anti-cancer drugs</title><addtitle>Anticancer Drugs</addtitle><description>The objective of this study was to evaluate extracellular matrix metalloproteinase (EMMPRIN) as a novel target in orthotopic pancreatic cancer murine models. MIA PaCa-2 human pancreatic tumor cells were implanted in groups 1 and 3–7, whereas MIA PaCa-2 EMMPRIN knockdown cells were implanted in group 2. Dosing with anti-EMMPRIN antibody started immediately after implantation for groups 1–3 (residual tumor model) and at 21 days after cell implantation for groups 4–7 (established tumor model). Groups 3, 5, and 7 were treated with anti-EMMRPIN antibody (0.2–1.0 mg) twice weekly for 2–3 weeks, whereas the other groups served as the control. In the residual tumor model, tumor growth of anti-EMMPRIN-treated group was successfully arrested for 21 days (15±4 mm), which was significantly lower than that of the EMMPRIN knockdown group (80±15 mm; P=0.001) or the control group (240±41 mm; P<0.001). In the established tumor model, anti-EMMPRIN therapy lowered tumor volume increase by approximately 40% compared with the control, regardless of the dose amount. Ki67-expressed cell density of group 5 was 939±150 mm, which was significantly lower than that of group 4 (1709±145 mm; P=0.006). Microvessel density of group 5 (30±6 mm) was also significantly lower than that of group 4 (53±5 mm; P=0.014), whereas the microvessel size of group 5 (191±22 μm) was significantly larger than that of group 4 (113±26 μm; P=0.049). These data show the high potential of anti-EMMPRIN therapy for pancreatic cancer and support its clinical translation.</description><subject>Animals</subject><subject>Antibodies, Anti-Idiotypic - immunology</subject><subject>Antibodies, Anti-Idiotypic - pharmacology</subject><subject>Antibodies, Monoclonal, Murine-Derived - immunology</subject><subject>Antibodies, Monoclonal, Murine-Derived - therapeutic use</subject><subject>Basigin - biosynthesis</subject><subject>Basigin - immunology</subject><subject>Basigin - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Drug Evaluation, Preclinical</subject><subject>Extracellular Matrix - metabolism</subject><subject>Female</subject><subject>Gene Knockdown Techniques</subject><subject>Humans</subject><subject>Ki-67 Antigen - biosynthesis</subject><subject>Ki-67 Antigen - metabolism</subject><subject>Matrix Metalloproteinases - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, SCID</subject><subject>Molecular Targeted Therapy</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Radioimmunoassay</subject><subject>Tumor Burden - drug effects</subject><subject>Xenograft Model Antitumor Assays</subject><issn>0959-4973</issn><issn>1473-5741</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFO3DAQhi3UCrZb3gBVvvUUOo7txD6uttsWCamXco4mzoQNOJvFdgq8PUYLPXCgl5nR6JuZf37GzgScC7D1t_Xq-zm0ICTJ0khlpRB0xBZC1bLQtRIf2AKstoWytTxhn2K8AYDcl8fspBS1BFOKBbvaPKSAjryfMfARUxge-EgJvZ_2YUo07DASx8iR76a_5HnCcE2J91Pge9y5QJgGx10uKfC0pYD7x8_sY48-0ulLXrKrH5s_61_F5e-fF-vVZeGUlFS0HWhtqKykJSqVM33f9p2TqgINplN9lSO1bX4Xs15ju1aDQAOdcJ0DkEv29bA3S72bKaZmHOLzM7ijaY6NsVbIWoP8P2kqbeta6EyqA-nCFGOgvtmHYcTw2Ahonp1vsvPNW-fz2JeXA3M7Uvdv6NXqDJgDcD_5RCHe-vmeQrMl9Gn7_u4nweGSMg</recordid><startdate>201110</startdate><enddate>201110</enddate><creator>Kim, Hyunki</creator><creator>Zhai, Guihua</creator><creator>Liu, Zhiyong</creator><creator>Samuel, Sharon</creator><creator>Shah, Nemil</creator><creator>Helman, Emily E</creator><creator>Knowles, Joseph A</creator><creator>Stockard, Cecil R</creator><creator>Fineberg, Naomi S</creator><creator>Grizzle, William E</creator><creator>Zhou, Tong</creator><creator>Zinn, Kurt R</creator><creator>Rosenthal, Eben L</creator><general>Lippincott Williams & Wilkins, Inc</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>7X8</scope><scope>7TO</scope><scope>7U7</scope><scope>C1K</scope><scope>H94</scope></search><sort><creationdate>201110</creationdate><title>Extracelluar matrix metalloproteinase as a novel target for pancreatic cancer therapy</title><author>Kim, Hyunki ; Zhai, Guihua ; Liu, Zhiyong ; Samuel, Sharon ; Shah, Nemil ; Helman, Emily E ; Knowles, Joseph A ; Stockard, Cecil R ; Fineberg, Naomi S ; Grizzle, William E ; Zhou, Tong ; Zinn, Kurt R ; Rosenthal, Eben L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433e-bd0558e2639ee24c8ffbfdc3460508d4f608debb097a30889db501a80d1cdc003</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>Antibodies, Anti-Idiotypic - immunology</topic><topic>Antibodies, Anti-Idiotypic - pharmacology</topic><topic>Antibodies, Monoclonal, Murine-Derived - immunology</topic><topic>Antibodies, Monoclonal, Murine-Derived - therapeutic use</topic><topic>Basigin - biosynthesis</topic><topic>Basigin - immunology</topic><topic>Basigin - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Drug Evaluation, Preclinical</topic><topic>Extracellular Matrix - metabolism</topic><topic>Female</topic><topic>Gene Knockdown Techniques</topic><topic>Humans</topic><topic>Ki-67 Antigen - biosynthesis</topic><topic>Ki-67 Antigen - metabolism</topic><topic>Matrix Metalloproteinases - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, SCID</topic><topic>Molecular Targeted Therapy</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Radioimmunoassay</topic><topic>Tumor Burden - drug effects</topic><topic>Xenograft Model Antitumor Assays</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Hyunki</creatorcontrib><creatorcontrib>Zhai, Guihua</creatorcontrib><creatorcontrib>Liu, Zhiyong</creatorcontrib><creatorcontrib>Samuel, Sharon</creatorcontrib><creatorcontrib>Shah, Nemil</creatorcontrib><creatorcontrib>Helman, Emily E</creatorcontrib><creatorcontrib>Knowles, Joseph A</creatorcontrib><creatorcontrib>Stockard, Cecil R</creatorcontrib><creatorcontrib>Fineberg, Naomi S</creatorcontrib><creatorcontrib>Grizzle, William E</creatorcontrib><creatorcontrib>Zhou, Tong</creatorcontrib><creatorcontrib>Zinn, Kurt R</creatorcontrib><creatorcontrib>Rosenthal, Eben L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Anti-cancer drugs</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Hyunki</au><au>Zhai, Guihua</au><au>Liu, Zhiyong</au><au>Samuel, Sharon</au><au>Shah, Nemil</au><au>Helman, Emily E</au><au>Knowles, Joseph A</au><au>Stockard, Cecil R</au><au>Fineberg, Naomi S</au><au>Grizzle, William E</au><au>Zhou, Tong</au><au>Zinn, Kurt R</au><au>Rosenthal, Eben L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Extracelluar matrix metalloproteinase as a novel target for pancreatic cancer therapy</atitle><jtitle>Anti-cancer drugs</jtitle><addtitle>Anticancer Drugs</addtitle><date>2011-10</date><risdate>2011</risdate><volume>22</volume><issue>9</issue><spage>864</spage><epage>874</epage><pages>864-874</pages><issn>0959-4973</issn><eissn>1473-5741</eissn><abstract>The objective of this study was to evaluate extracellular matrix metalloproteinase (EMMPRIN) as a novel target in orthotopic pancreatic cancer murine models. MIA PaCa-2 human pancreatic tumor cells were implanted in groups 1 and 3–7, whereas MIA PaCa-2 EMMPRIN knockdown cells were implanted in group 2. Dosing with anti-EMMPRIN antibody started immediately after implantation for groups 1–3 (residual tumor model) and at 21 days after cell implantation for groups 4–7 (established tumor model). Groups 3, 5, and 7 were treated with anti-EMMRPIN antibody (0.2–1.0 mg) twice weekly for 2–3 weeks, whereas the other groups served as the control. In the residual tumor model, tumor growth of anti-EMMPRIN-treated group was successfully arrested for 21 days (15±4 mm), which was significantly lower than that of the EMMPRIN knockdown group (80±15 mm; P=0.001) or the control group (240±41 mm; P<0.001). In the established tumor model, anti-EMMPRIN therapy lowered tumor volume increase by approximately 40% compared with the control, regardless of the dose amount. Ki67-expressed cell density of group 5 was 939±150 mm, which was significantly lower than that of group 4 (1709±145 mm; P=0.006). Microvessel density of group 5 (30±6 mm) was also significantly lower than that of group 4 (53±5 mm; P=0.014), whereas the microvessel size of group 5 (191±22 μm) was significantly larger than that of group 4 (113±26 μm; P=0.049). These data show the high potential of anti-EMMPRIN therapy for pancreatic cancer and support its clinical translation.</abstract><cop>England</cop><pub>Lippincott Williams & Wilkins, Inc</pub><pmid>21730821</pmid><doi>10.1097/CAD.0b013e328349311e</doi><tpages>11</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies, Anti-Idiotypic - immunology Antibodies, Anti-Idiotypic - pharmacology Antibodies, Monoclonal, Murine-Derived - immunology Antibodies, Monoclonal, Murine-Derived - therapeutic use Basigin - biosynthesis Basigin - immunology Basigin - metabolism Cell Line, Tumor Drug Evaluation, Preclinical Extracellular Matrix - metabolism Female Gene Knockdown Techniques Humans Ki-67 Antigen - biosynthesis Ki-67 Antigen - metabolism Matrix Metalloproteinases - metabolism Mice Mice, Inbred BALB C Mice, SCID Molecular Targeted Therapy Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - metabolism Pancreatic Neoplasms - pathology Radioimmunoassay Tumor Burden - drug effects Xenograft Model Antitumor Assays |
| title | Extracelluar matrix metalloproteinase as a novel target for pancreatic cancer therapy |
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