Silencing of X-linked Inhibitor of Apoptosis (XIAP) Decreases Gemcitabine Resistance of Pancreatic Cancer Cells
Background: The X-linked inhibitor of apoptosis (XIAP) belongs to a family of proteins that suppresses apoptosis by inhibition of caspases in some cancers. It confers resistance to apoptosis induction by chemotherapeutic agents. The aim of this study was to evaluate the influence of XIAP in pancreat...
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| Veröffentlicht in: | Anticancer research 2006-09, Vol.26 (5A), p.3265-3273 |
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| creator | SHRIKHANDE, Shailesh V KLEEFF, Jorg KAYED, Hany KELEG, Shereen REISER, Carolin GIESE, Thomas BUCHLER, Markus W ESPOSITO, Irene FRIESS, Helmut |
| description | Background: The X-linked inhibitor of apoptosis (XIAP) belongs to a family of proteins that suppresses apoptosis by inhibition
of caspases in some cancers. It confers resistance to apoptosis induction by chemotherapeutic agents. The aim of this study
was to evaluate the influence of XIAP in pancreatic cancer. Patients and Methods: Tissue samples from 43 patients with pancreatic
adenocarcinoma (median age of 67 years, range from 39-81 years) were analyzed. Pancreatic samples from healthy organ donors
(10) and chronic pancreatitis patients (10) served as controls. XIAP expression and localization analysis was carried out
by quantitative RT-PCR and immunohistochemistry (IHC). XIAP silencing was achieved by transfection of specifically designed
siRNA oligonucleotides. Proliferation and chemotherapy experiments were performed by MTT cell growth assays. Results: There
was a 2.1-fold increase of median XIAP mRNA levels in pancreatic cancers compared to controls. Kaplan-Meier analysis indicated
a tendency for reduced patient survival with increasing levels of XIAP mRNA (higher levels: 13.4 months; lower levels: 16.1
months). IHC revealed strong XIAP staining in tubular complexes and pancreatic cancer cells. XIAP silencing resulted in a
slight reduction of the proliferation of Capan-1 and T3M4 pancreatic cancer cells. In addition, XIAP silencing resulted in
increased sensitivity of both cell lines to gemcitabine. Conclusion: XIAP is overexpressed in pancreatic cancer and contributes
to chemoresistance. Interfering with this pathway may have potential therapeutic role in the treatment of this disease. |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_pasca</sourceid><recordid>TN_cdi_pubmed_primary_17094439</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>17094439</sourcerecordid><originalsourceid>FETCH-LOGICAL-h270t-a78b04b7c6d1540edb7a2c101b422c801026dc5f04db41e261db12980cc9e0373</originalsourceid><addsrcrecordid>eNpFj11LwzAUhosobk7_guRG0YvCyVfTXpapczBw-AG7K0martH0g6Qi_ns7N_HqHF6e83Deo2iKRYZjwSkcR1MgHGIBwCfRWQjvAEmSpfQ0mmABGWM0m0bdi3Wm1bbdoq5Cm9jZ9sOUaNnWVtmh87s077t-6IIN6GazzNe36M5ob2QwAS1Mo-0glW0NejYjMshWm93RelxGaLAazXeZR3PjXDiPTirpgrk4zFn09nD_On-MV0-L5TxfxTURMMRSpAqYEjopMWdgSiUk0RiwYoToFDCQpNS8AlYqhg1JcKkwyVLQOjNABZ1Fl3tv_6kaUxa9t43038Vf8xG4OgAyaOkqPz5pwz-XEsb5r-h6z9V2W39Zb4rQSOdGLS2kJ0nB84KShNMfHttvPg</addsrcrecordid><sourcetype>Index Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Silencing of X-linked Inhibitor of Apoptosis (XIAP) Decreases Gemcitabine Resistance of Pancreatic Cancer Cells</title><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>SHRIKHANDE, Shailesh V ; KLEEFF, Jorg ; KAYED, Hany ; KELEG, Shereen ; REISER, Carolin ; GIESE, Thomas ; BUCHLER, Markus W ; ESPOSITO, Irene ; FRIESS, Helmut</creator><creatorcontrib>SHRIKHANDE, Shailesh V ; KLEEFF, Jorg ; KAYED, Hany ; KELEG, Shereen ; REISER, Carolin ; GIESE, Thomas ; BUCHLER, Markus W ; ESPOSITO, Irene ; FRIESS, Helmut</creatorcontrib><description>Background: The X-linked inhibitor of apoptosis (XIAP) belongs to a family of proteins that suppresses apoptosis by inhibition
of caspases in some cancers. It confers resistance to apoptosis induction by chemotherapeutic agents. The aim of this study
was to evaluate the influence of XIAP in pancreatic cancer. Patients and Methods: Tissue samples from 43 patients with pancreatic
adenocarcinoma (median age of 67 years, range from 39-81 years) were analyzed. Pancreatic samples from healthy organ donors
(10) and chronic pancreatitis patients (10) served as controls. XIAP expression and localization analysis was carried out
by quantitative RT-PCR and immunohistochemistry (IHC). XIAP silencing was achieved by transfection of specifically designed
siRNA oligonucleotides. Proliferation and chemotherapy experiments were performed by MTT cell growth assays. Results: There
was a 2.1-fold increase of median XIAP mRNA levels in pancreatic cancers compared to controls. Kaplan-Meier analysis indicated
a tendency for reduced patient survival with increasing levels of XIAP mRNA (higher levels: 13.4 months; lower levels: 16.1
months). IHC revealed strong XIAP staining in tubular complexes and pancreatic cancer cells. XIAP silencing resulted in a
slight reduction of the proliferation of Capan-1 and T3M4 pancreatic cancer cells. In addition, XIAP silencing resulted in
increased sensitivity of both cell lines to gemcitabine. Conclusion: XIAP is overexpressed in pancreatic cancer and contributes
to chemoresistance. Interfering with this pathway may have potential therapeutic role in the treatment of this disease.</description><identifier>ISSN: 0250-7005</identifier><identifier>EISSN: 1791-7530</identifier><identifier>PMID: 17094439</identifier><language>eng</language><publisher>Attiki: International Institute of Anticancer Research</publisher><subject>Adolescent ; Adult ; Aged ; Aged, 80 and over ; Antimetabolites, Antineoplastic - therapeutic use ; Apoptosis ; Biological and medical sciences ; Carcinoma, Pancreatic Ductal - drug therapy ; Carcinoma, Pancreatic Ductal - genetics ; Carcinoma, Pancreatic Ductal - metabolism ; Case-Control Studies ; Caspases - metabolism ; Cell Line, Tumor ; Cell Proliferation ; Deoxycytidine - analogs & derivatives ; Deoxycytidine - therapeutic use ; Drug Resistance, Neoplasm - genetics ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Gene Silencing ; Humans ; Immunoblotting ; Immunoenzyme Techniques ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Middle Aged ; Pancreas - metabolism ; Pancreatic Neoplasms - drug therapy ; Pancreatic Neoplasms - genetics ; Pancreatic Neoplasms - metabolism ; Pancreatitis, Chronic - drug therapy ; Pancreatitis, Chronic - genetics ; Pancreatitis, Chronic - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; RNA, Small Interfering - pharmacology ; Survival Rate ; Tumors ; X-Linked Inhibitor of Apoptosis Protein - antagonists & inhibitors ; X-Linked Inhibitor of Apoptosis Protein - genetics ; X-Linked Inhibitor of Apoptosis Protein - metabolism</subject><ispartof>Anticancer research, 2006-09, Vol.26 (5A), p.3265-3273</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18245537$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17094439$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHRIKHANDE, Shailesh V</creatorcontrib><creatorcontrib>KLEEFF, Jorg</creatorcontrib><creatorcontrib>KAYED, Hany</creatorcontrib><creatorcontrib>KELEG, Shereen</creatorcontrib><creatorcontrib>REISER, Carolin</creatorcontrib><creatorcontrib>GIESE, Thomas</creatorcontrib><creatorcontrib>BUCHLER, Markus W</creatorcontrib><creatorcontrib>ESPOSITO, Irene</creatorcontrib><creatorcontrib>FRIESS, Helmut</creatorcontrib><title>Silencing of X-linked Inhibitor of Apoptosis (XIAP) Decreases Gemcitabine Resistance of Pancreatic Cancer Cells</title><title>Anticancer research</title><addtitle>Anticancer Res</addtitle><description>Background: The X-linked inhibitor of apoptosis (XIAP) belongs to a family of proteins that suppresses apoptosis by inhibition
of caspases in some cancers. It confers resistance to apoptosis induction by chemotherapeutic agents. The aim of this study
was to evaluate the influence of XIAP in pancreatic cancer. Patients and Methods: Tissue samples from 43 patients with pancreatic
adenocarcinoma (median age of 67 years, range from 39-81 years) were analyzed. Pancreatic samples from healthy organ donors
(10) and chronic pancreatitis patients (10) served as controls. XIAP expression and localization analysis was carried out
by quantitative RT-PCR and immunohistochemistry (IHC). XIAP silencing was achieved by transfection of specifically designed
siRNA oligonucleotides. Proliferation and chemotherapy experiments were performed by MTT cell growth assays. Results: There
was a 2.1-fold increase of median XIAP mRNA levels in pancreatic cancers compared to controls. Kaplan-Meier analysis indicated
a tendency for reduced patient survival with increasing levels of XIAP mRNA (higher levels: 13.4 months; lower levels: 16.1
months). IHC revealed strong XIAP staining in tubular complexes and pancreatic cancer cells. XIAP silencing resulted in a
slight reduction of the proliferation of Capan-1 and T3M4 pancreatic cancer cells. In addition, XIAP silencing resulted in
increased sensitivity of both cell lines to gemcitabine. Conclusion: XIAP is overexpressed in pancreatic cancer and contributes
to chemoresistance. Interfering with this pathway may have potential therapeutic role in the treatment of this disease.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Antimetabolites, Antineoplastic - therapeutic use</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Carcinoma, Pancreatic Ductal - drug therapy</subject><subject>Carcinoma, Pancreatic Ductal - genetics</subject><subject>Carcinoma, Pancreatic Ductal - metabolism</subject><subject>Case-Control Studies</subject><subject>Caspases - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Deoxycytidine - therapeutic use</subject><subject>Drug Resistance, Neoplasm - genetics</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Gene Silencing</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunoenzyme Techniques</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pancreas - metabolism</subject><subject>Pancreatic Neoplasms - drug therapy</subject><subject>Pancreatic Neoplasms - genetics</subject><subject>Pancreatic Neoplasms - metabolism</subject><subject>Pancreatitis, Chronic - drug therapy</subject><subject>Pancreatitis, Chronic - genetics</subject><subject>Pancreatitis, Chronic - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>RNA, Small Interfering - pharmacology</subject><subject>Survival Rate</subject><subject>Tumors</subject><subject>X-Linked Inhibitor of Apoptosis Protein - antagonists & inhibitors</subject><subject>X-Linked Inhibitor of Apoptosis Protein - genetics</subject><subject>X-Linked Inhibitor of Apoptosis Protein - metabolism</subject><issn>0250-7005</issn><issn>1791-7530</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFj11LwzAUhosobk7_guRG0YvCyVfTXpapczBw-AG7K0martH0g6Qi_ns7N_HqHF6e83Deo2iKRYZjwSkcR1MgHGIBwCfRWQjvAEmSpfQ0mmABGWM0m0bdi3Wm1bbdoq5Cm9jZ9sOUaNnWVtmh87s077t-6IIN6GazzNe36M5ob2QwAS1Mo-0glW0NejYjMshWm93RelxGaLAazXeZR3PjXDiPTirpgrk4zFn09nD_On-MV0-L5TxfxTURMMRSpAqYEjopMWdgSiUk0RiwYoToFDCQpNS8AlYqhg1JcKkwyVLQOjNABZ1Fl3tv_6kaUxa9t43038Vf8xG4OgAyaOkqPz5pwz-XEsb5r-h6z9V2W39Zb4rQSOdGLS2kJ0nB84KShNMfHttvPg</recordid><startdate>20060901</startdate><enddate>20060901</enddate><creator>SHRIKHANDE, Shailesh V</creator><creator>KLEEFF, Jorg</creator><creator>KAYED, Hany</creator><creator>KELEG, Shereen</creator><creator>REISER, Carolin</creator><creator>GIESE, Thomas</creator><creator>BUCHLER, Markus W</creator><creator>ESPOSITO, Irene</creator><creator>FRIESS, Helmut</creator><general>International Institute of Anticancer Research</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>20060901</creationdate><title>Silencing of X-linked Inhibitor of Apoptosis (XIAP) Decreases Gemcitabine Resistance of Pancreatic Cancer Cells</title><author>SHRIKHANDE, Shailesh V ; KLEEFF, Jorg ; KAYED, Hany ; KELEG, Shereen ; REISER, Carolin ; GIESE, Thomas ; BUCHLER, Markus W ; ESPOSITO, Irene ; FRIESS, Helmut</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h270t-a78b04b7c6d1540edb7a2c101b422c801026dc5f04db41e261db12980cc9e0373</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Antimetabolites, Antineoplastic - therapeutic use</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Carcinoma, Pancreatic Ductal - drug therapy</topic><topic>Carcinoma, Pancreatic Ductal - genetics</topic><topic>Carcinoma, Pancreatic Ductal - metabolism</topic><topic>Case-Control Studies</topic><topic>Caspases - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Deoxycytidine - therapeutic use</topic><topic>Drug Resistance, Neoplasm - genetics</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Gene Silencing</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunoenzyme Techniques</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pancreas - metabolism</topic><topic>Pancreatic Neoplasms - drug therapy</topic><topic>Pancreatic Neoplasms - genetics</topic><topic>Pancreatic Neoplasms - metabolism</topic><topic>Pancreatitis, Chronic - drug therapy</topic><topic>Pancreatitis, Chronic - genetics</topic><topic>Pancreatitis, Chronic - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>RNA, Small Interfering - pharmacology</topic><topic>Survival Rate</topic><topic>Tumors</topic><topic>X-Linked Inhibitor of Apoptosis Protein - antagonists & inhibitors</topic><topic>X-Linked Inhibitor of Apoptosis Protein - genetics</topic><topic>X-Linked Inhibitor of Apoptosis Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHRIKHANDE, Shailesh V</creatorcontrib><creatorcontrib>KLEEFF, Jorg</creatorcontrib><creatorcontrib>KAYED, Hany</creatorcontrib><creatorcontrib>KELEG, Shereen</creatorcontrib><creatorcontrib>REISER, Carolin</creatorcontrib><creatorcontrib>GIESE, Thomas</creatorcontrib><creatorcontrib>BUCHLER, Markus W</creatorcontrib><creatorcontrib>ESPOSITO, Irene</creatorcontrib><creatorcontrib>FRIESS, Helmut</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Anticancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHRIKHANDE, Shailesh V</au><au>KLEEFF, Jorg</au><au>KAYED, Hany</au><au>KELEG, Shereen</au><au>REISER, Carolin</au><au>GIESE, Thomas</au><au>BUCHLER, Markus W</au><au>ESPOSITO, Irene</au><au>FRIESS, Helmut</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silencing of X-linked Inhibitor of Apoptosis (XIAP) Decreases Gemcitabine Resistance of Pancreatic Cancer Cells</atitle><jtitle>Anticancer research</jtitle><addtitle>Anticancer Res</addtitle><date>2006-09-01</date><risdate>2006</risdate><volume>26</volume><issue>5A</issue><spage>3265</spage><epage>3273</epage><pages>3265-3273</pages><issn>0250-7005</issn><eissn>1791-7530</eissn><abstract>Background: The X-linked inhibitor of apoptosis (XIAP) belongs to a family of proteins that suppresses apoptosis by inhibition
of caspases in some cancers. It confers resistance to apoptosis induction by chemotherapeutic agents. The aim of this study
was to evaluate the influence of XIAP in pancreatic cancer. Patients and Methods: Tissue samples from 43 patients with pancreatic
adenocarcinoma (median age of 67 years, range from 39-81 years) were analyzed. Pancreatic samples from healthy organ donors
(10) and chronic pancreatitis patients (10) served as controls. XIAP expression and localization analysis was carried out
by quantitative RT-PCR and immunohistochemistry (IHC). XIAP silencing was achieved by transfection of specifically designed
siRNA oligonucleotides. Proliferation and chemotherapy experiments were performed by MTT cell growth assays. Results: There
was a 2.1-fold increase of median XIAP mRNA levels in pancreatic cancers compared to controls. Kaplan-Meier analysis indicated
a tendency for reduced patient survival with increasing levels of XIAP mRNA (higher levels: 13.4 months; lower levels: 16.1
months). IHC revealed strong XIAP staining in tubular complexes and pancreatic cancer cells. XIAP silencing resulted in a
slight reduction of the proliferation of Capan-1 and T3M4 pancreatic cancer cells. In addition, XIAP silencing resulted in
increased sensitivity of both cell lines to gemcitabine. Conclusion: XIAP is overexpressed in pancreatic cancer and contributes
to chemoresistance. Interfering with this pathway may have potential therapeutic role in the treatment of this disease.</abstract><cop>Attiki</cop><pub>International Institute of Anticancer Research</pub><pmid>17094439</pmid><tpages>9</tpages></addata></record> |
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| subjects | Adolescent Adult Aged Aged, 80 and over Antimetabolites, Antineoplastic - therapeutic use Apoptosis Biological and medical sciences Carcinoma, Pancreatic Ductal - drug therapy Carcinoma, Pancreatic Ductal - genetics Carcinoma, Pancreatic Ductal - metabolism Case-Control Studies Caspases - metabolism Cell Line, Tumor Cell Proliferation Deoxycytidine - analogs & derivatives Deoxycytidine - therapeutic use Drug Resistance, Neoplasm - genetics Female Gastroenterology. Liver. Pancreas. Abdomen Gene Silencing Humans Immunoblotting Immunoenzyme Techniques Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Middle Aged Pancreas - metabolism Pancreatic Neoplasms - drug therapy Pancreatic Neoplasms - genetics Pancreatic Neoplasms - metabolism Pancreatitis, Chronic - drug therapy Pancreatitis, Chronic - genetics Pancreatitis, Chronic - metabolism Reverse Transcriptase Polymerase Chain Reaction RNA, Messenger - genetics RNA, Messenger - metabolism RNA, Small Interfering - pharmacology Survival Rate Tumors X-Linked Inhibitor of Apoptosis Protein - antagonists & inhibitors X-Linked Inhibitor of Apoptosis Protein - genetics X-Linked Inhibitor of Apoptosis Protein - metabolism |
| title | Silencing of X-linked Inhibitor of Apoptosis (XIAP) Decreases Gemcitabine Resistance of Pancreatic Cancer Cells |
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