Regulation of Multidrug Resistance by MGr1-Antigen in Gastric Cancer Cells
Previously, a novel protein, MGr1-Ag, was associated with tumor multidrug resistance (MDR), and the role and the underlying mechanisms of MGr1-Ag in MDR of gastric cancer cells were characterized. Initial studies using the introduction of sense or antisense vectors for MGr1-Ag resulted in the geneti...
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| Veröffentlicht in: | Tumor biology 2006-01, Vol.27 (1), p.27-35 |
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| creator | Sun, Li Shi, Yongquan Guo, Changcun Yao, Liping Lin, Tao Du, Jingping Han, Quanli Han, Ying Fan, Daiming |
| description | Previously, a novel protein, MGr1-Ag, was associated with tumor multidrug resistance (MDR), and the role and the underlying mechanisms of MGr1-Ag in MDR of gastric cancer cells were characterized. Initial studies using the introduction of sense or antisense vectors for MGr1-Ag resulted in the genetical up- or downregulation of MGr1-Ag in gastric cancer cells, respectively. Subsequent studies revealed the expression of MGr1-Ag, P-glycoprotein (P-gp), MDR-associated protein (MRP), Bcl-2 and Bax in gastric cancer cells via Western blot analysis. The sensitivity of gastric cancer cells to chemotherapeutic drugs was assessed using the colony-forming assay, and Adriamycin (ADM) accumulation was evaluated by flow cytometry. Further study of ADM-induced apoptosis was detected by annexin-V/propidium iodide staining. The expression level of MGr1-Ag in MDR gastric cancer cells is much higher than that in their parental cells. Overexpression of exogenous MGr1-Ag may promote the MDR phenotype of gastric cancer cells, decrease intracellular ADM accumulation and protect gastric cancer cells from ADM-induced apoptosis, whereas downregulation of MGr1-Ag had reverse effects. Western blot analysis suggested that MGr1-Ag may regulate the expression of P-gp, MRP, Bcl-2 and Bax. In conclusion, MGr1-Ag may promote MDR of gastric cancer cells via a decrease in intracellular drug accumulation and inhibition of drug-induced apoptosis. |
| doi_str_mv | 10.1159/000090153 |
| format | Article |
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Initial studies using the introduction of sense or antisense vectors for MGr1-Ag resulted in the genetical up- or downregulation of MGr1-Ag in gastric cancer cells, respectively. Subsequent studies revealed the expression of MGr1-Ag, P-glycoprotein (P-gp), MDR-associated protein (MRP), Bcl-2 and Bax in gastric cancer cells via Western blot analysis. The sensitivity of gastric cancer cells to chemotherapeutic drugs was assessed using the colony-forming assay, and Adriamycin (ADM) accumulation was evaluated by flow cytometry. Further study of ADM-induced apoptosis was detected by annexin-V/propidium iodide staining. The expression level of MGr1-Ag in MDR gastric cancer cells is much higher than that in their parental cells. Overexpression of exogenous MGr1-Ag may promote the MDR phenotype of gastric cancer cells, decrease intracellular ADM accumulation and protect gastric cancer cells from ADM-induced apoptosis, whereas downregulation of MGr1-Ag had reverse effects. Western blot analysis suggested that MGr1-Ag may regulate the expression of P-gp, MRP, Bcl-2 and Bax. In conclusion, MGr1-Ag may promote MDR of gastric cancer cells via a decrease in intracellular drug accumulation and inhibition of drug-induced apoptosis.</description><identifier>ISSN: 1010-4283</identifier><identifier>EISSN: 1423-0380</identifier><identifier>DOI: 10.1159/000090153</identifier><identifier>PMID: 16340247</identifier><language>eng</language><publisher>Basel, Switzerland: Springer Nature B.V</publisher><subject>Antibiotics, Antineoplastic - pharmacokinetics ; Antibiotics, Antineoplastic - pharmacology ; Antigens, Neoplasm - biosynthesis ; Antigens, Neoplasm - physiology ; Apoptosis - drug effects ; Blotting, Western ; Down-Regulation ; Doxorubicin - pharmacokinetics ; Doxorubicin - pharmacology ; Drug Resistance, Multiple - genetics ; Flow Cytometry ; Humans ; Phenotype ; Research Article ; Stomach Neoplasms - genetics ; Stomach Neoplasms - pathology ; Tumor Cells, Cultured</subject><ispartof>Tumor biology, 2006-01, Vol.27 (1), p.27-35</ispartof><rights>2006 S. Karger AG, Basel</rights><rights>Copyright 2006 S. Karger AG, Basel.</rights><rights>Copyright (c) 2006 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c330t-b3e836ed63edf50b4504c52652e13482abe11925ac64fe35899f12ee98fa97db3</citedby><cites>FETCH-LOGICAL-c330t-b3e836ed63edf50b4504c52652e13482abe11925ac64fe35899f12ee98fa97db3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,2422,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16340247$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sun, Li</creatorcontrib><creatorcontrib>Shi, Yongquan</creatorcontrib><creatorcontrib>Guo, Changcun</creatorcontrib><creatorcontrib>Yao, Liping</creatorcontrib><creatorcontrib>Lin, Tao</creatorcontrib><creatorcontrib>Du, Jingping</creatorcontrib><creatorcontrib>Han, Quanli</creatorcontrib><creatorcontrib>Han, Ying</creatorcontrib><creatorcontrib>Fan, Daiming</creatorcontrib><title>Regulation of Multidrug Resistance by MGr1-Antigen in Gastric Cancer Cells</title><title>Tumor biology</title><addtitle>Tumor Biol</addtitle><description>Previously, a novel protein, MGr1-Ag, was associated with tumor multidrug resistance (MDR), and the role and the underlying mechanisms of MGr1-Ag in MDR of gastric cancer cells were characterized. Initial studies using the introduction of sense or antisense vectors for MGr1-Ag resulted in the genetical up- or downregulation of MGr1-Ag in gastric cancer cells, respectively. Subsequent studies revealed the expression of MGr1-Ag, P-glycoprotein (P-gp), MDR-associated protein (MRP), Bcl-2 and Bax in gastric cancer cells via Western blot analysis. The sensitivity of gastric cancer cells to chemotherapeutic drugs was assessed using the colony-forming assay, and Adriamycin (ADM) accumulation was evaluated by flow cytometry. Further study of ADM-induced apoptosis was detected by annexin-V/propidium iodide staining. The expression level of MGr1-Ag in MDR gastric cancer cells is much higher than that in their parental cells. Overexpression of exogenous MGr1-Ag may promote the MDR phenotype of gastric cancer cells, decrease intracellular ADM accumulation and protect gastric cancer cells from ADM-induced apoptosis, whereas downregulation of MGr1-Ag had reverse effects. Western blot analysis suggested that MGr1-Ag may regulate the expression of P-gp, MRP, Bcl-2 and Bax. In conclusion, MGr1-Ag may promote MDR of gastric cancer cells via a decrease in intracellular drug accumulation and inhibition of drug-induced apoptosis.</description><subject>Antibiotics, Antineoplastic - pharmacokinetics</subject><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Antigens, Neoplasm - biosynthesis</subject><subject>Antigens, Neoplasm - physiology</subject><subject>Apoptosis - drug effects</subject><subject>Blotting, Western</subject><subject>Down-Regulation</subject><subject>Doxorubicin - pharmacokinetics</subject><subject>Doxorubicin - pharmacology</subject><subject>Drug Resistance, Multiple - genetics</subject><subject>Flow Cytometry</subject><subject>Humans</subject><subject>Phenotype</subject><subject>Research Article</subject><subject>Stomach Neoplasms - genetics</subject><subject>Stomach Neoplasms - pathology</subject><subject>Tumor Cells, Cultured</subject><issn>1010-4283</issn><issn>1423-0380</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpd0E1Lw0AQBuBFFFurB8-CLB4ED9H9zu6xBK1Ki1D0HDbJpKSmSd1NDv33bkmp4FxmDs8Mw4vQNSWPlErzREIZQiU_QWMqGI8I1-Q0zISSSDDNR-jC-zUJxBh1jkZUcUGYiMfofQmrvrZd1Ta4LfGir7uqcP0KL8FXvrNNDjjb4cXM0WjadNUKGlw1eGZ956ocJ3vgcAJ17S_RWWlrD1eHPkFfL8-fyWs0_5i9JdN5lHNOuijjoLmCQnEoSkkyIYnIJVOSAeVCM5sBpYZJmytRApfamJIyAKNLa-Ii4xN0P9zduvanB9-lm8rn4QPbQNv7VMVSx7HWAd79g-u2d034LWWMxVwZYgJ6GFDuWu8dlOnWVRvrdikl6T7d9JhusLeHg322geJPHuIM4GYA39atwB3BsP4LE0B7Ag</recordid><startdate>20060101</startdate><enddate>20060101</enddate><creator>Sun, Li</creator><creator>Shi, Yongquan</creator><creator>Guo, Changcun</creator><creator>Yao, Liping</creator><creator>Lin, Tao</creator><creator>Du, Jingping</creator><creator>Han, Quanli</creator><creator>Han, Ying</creator><creator>Fan, Daiming</creator><general>Springer Nature B.V</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>7T5</scope><scope>7TO</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope></search><sort><creationdate>20060101</creationdate><title>Regulation of Multidrug Resistance by MGr1-Antigen in Gastric Cancer Cells</title><author>Sun, Li ; Shi, Yongquan ; Guo, Changcun ; Yao, Liping ; Lin, Tao ; Du, Jingping ; Han, Quanli ; Han, Ying ; Fan, Daiming</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c330t-b3e836ed63edf50b4504c52652e13482abe11925ac64fe35899f12ee98fa97db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Antibiotics, Antineoplastic - 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Academic</collection><jtitle>Tumor biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sun, Li</au><au>Shi, Yongquan</au><au>Guo, Changcun</au><au>Yao, Liping</au><au>Lin, Tao</au><au>Du, Jingping</au><au>Han, Quanli</au><au>Han, Ying</au><au>Fan, Daiming</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Multidrug Resistance by MGr1-Antigen in Gastric Cancer Cells</atitle><jtitle>Tumor biology</jtitle><addtitle>Tumor Biol</addtitle><date>2006-01-01</date><risdate>2006</risdate><volume>27</volume><issue>1</issue><spage>27</spage><epage>35</epage><pages>27-35</pages><issn>1010-4283</issn><eissn>1423-0380</eissn><abstract>Previously, a novel protein, MGr1-Ag, was associated with tumor multidrug resistance (MDR), and the role and the underlying mechanisms of MGr1-Ag in MDR of gastric cancer cells were characterized. Initial studies using the introduction of sense or antisense vectors for MGr1-Ag resulted in the genetical up- or downregulation of MGr1-Ag in gastric cancer cells, respectively. Subsequent studies revealed the expression of MGr1-Ag, P-glycoprotein (P-gp), MDR-associated protein (MRP), Bcl-2 and Bax in gastric cancer cells via Western blot analysis. The sensitivity of gastric cancer cells to chemotherapeutic drugs was assessed using the colony-forming assay, and Adriamycin (ADM) accumulation was evaluated by flow cytometry. Further study of ADM-induced apoptosis was detected by annexin-V/propidium iodide staining. The expression level of MGr1-Ag in MDR gastric cancer cells is much higher than that in their parental cells. Overexpression of exogenous MGr1-Ag may promote the MDR phenotype of gastric cancer cells, decrease intracellular ADM accumulation and protect gastric cancer cells from ADM-induced apoptosis, whereas downregulation of MGr1-Ag had reverse effects. Western blot analysis suggested that MGr1-Ag may regulate the expression of P-gp, MRP, Bcl-2 and Bax. In conclusion, MGr1-Ag may promote MDR of gastric cancer cells via a decrease in intracellular drug accumulation and inhibition of drug-induced apoptosis.</abstract><cop>Basel, Switzerland</cop><pub>Springer Nature B.V</pub><pmid>16340247</pmid><doi>10.1159/000090153</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antibiotics, Antineoplastic - pharmacokinetics Antibiotics, Antineoplastic - pharmacology Antigens, Neoplasm - biosynthesis Antigens, Neoplasm - physiology Apoptosis - drug effects Blotting, Western Down-Regulation Doxorubicin - pharmacokinetics Doxorubicin - pharmacology Drug Resistance, Multiple - genetics Flow Cytometry Humans Phenotype Research Article Stomach Neoplasms - genetics Stomach Neoplasms - pathology Tumor Cells, Cultured |
| title | Regulation of Multidrug Resistance by MGr1-Antigen in Gastric Cancer Cells |
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