Inhibition of Heme Oxygenase-1 Increases Responsiveness of Pancreatic Cancer Cells to Anticancer Treatment
Heme oxygenase-1 (HO-1) is believed to represent a key enzyme for the protection of cells against “stress.” Its overexpression in different types of human cancers supports the notion that HO-1 provides a growth advantage and contributes to cellular resistance against chemotherapy and radiotherapy. G...
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| Veröffentlicht in: | Clinical cancer research 2005-05, Vol.11 (10), p.3790-3798 |
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| creator | BERBERAT, Pascal O DAMBRAUSKAS, Zilvinas GULBINAS, Antanas GIESE, Thomas GIESE, Nathalia KÜNZLI, Beat AUTSCHBACH, Frank MEUER, Stefan BÜCHLER, Markus W FRIESS, Helmut |
| description | Heme oxygenase-1 (HO-1) is believed to represent a key enzyme for the protection of cells against “stress.” Its overexpression
in different types of human cancers supports the notion that HO-1 provides a growth advantage and contributes to cellular
resistance against chemotherapy and radiotherapy. Given the poor survival rates of patients with pancreatic cancer due to
its aggressive growth behavior and its exceptional resistance to all known forms of anticancer treatment, we have investigated
the expression of HO-1 in human pancreatic cancer cells growth behavior and prognosis. Expression of HO-1 was analyzed in
human pancreatic cancer samples in comparison with normal pancreas by quantitative PCR, Western blot, and confocal microscopy.
The influence of radiotherapy and chemotherapy on HO-1 expression in pancreatic cancer cell lines was evaluated. Furthermore,
HO-1 expression was specifically suppressed by small interfering RNA transfection and subsequently the alterations of growth
behavior and resistance to anticancer treatment were tested. Human pancreatic cancer showed a 6-fold and 3.5-fold HO-1 up-regulation
in comparison to normal pancreas based on mRNA and protein level, respectively ( P < 0.05). Cancer tissues revealed marked HO-1 immunoreactivity in tumor cells and in tumor associated immunocytes. Treatment
of the pancreatic cancer cell lines with gemcitabine or radiation strongly induced HO-1 expression. Targeted knockdown of
HO-1 expression led to pronounced growth inhibition of the pancreatic cancer cells and made tumor cells significantly more
sensitive to radiotherapy and chemotherapy. Therefore, specific inhibition of HO-1 expression may be a new option in pancreatic
cancer therapy and may be used as sensitizer to chemotherapy and radiotherapy. |
| doi_str_mv | 10.1158/1078-0432.CCR-04-2159 |
| format | Article |
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in different types of human cancers supports the notion that HO-1 provides a growth advantage and contributes to cellular
resistance against chemotherapy and radiotherapy. Given the poor survival rates of patients with pancreatic cancer due to
its aggressive growth behavior and its exceptional resistance to all known forms of anticancer treatment, we have investigated
the expression of HO-1 in human pancreatic cancer cells growth behavior and prognosis. Expression of HO-1 was analyzed in
human pancreatic cancer samples in comparison with normal pancreas by quantitative PCR, Western blot, and confocal microscopy.
The influence of radiotherapy and chemotherapy on HO-1 expression in pancreatic cancer cell lines was evaluated. Furthermore,
HO-1 expression was specifically suppressed by small interfering RNA transfection and subsequently the alterations of growth
behavior and resistance to anticancer treatment were tested. Human pancreatic cancer showed a 6-fold and 3.5-fold HO-1 up-regulation
in comparison to normal pancreas based on mRNA and protein level, respectively ( P < 0.05). Cancer tissues revealed marked HO-1 immunoreactivity in tumor cells and in tumor associated immunocytes. Treatment
of the pancreatic cancer cell lines with gemcitabine or radiation strongly induced HO-1 expression. Targeted knockdown of
HO-1 expression led to pronounced growth inhibition of the pancreatic cancer cells and made tumor cells significantly more
sensitive to radiotherapy and chemotherapy. Therefore, specific inhibition of HO-1 expression may be a new option in pancreatic
cancer therapy and may be used as sensitizer to chemotherapy and radiotherapy.</description><identifier>ISSN: 1078-0432</identifier><identifier>EISSN: 1557-3265</identifier><identifier>DOI: 10.1158/1078-0432.CCR-04-2159</identifier><identifier>PMID: 15897578</identifier><language>eng</language><publisher>Philadelphia, PA: American Association for Cancer Research</publisher><subject>Adult ; Aged ; anticancer therapy ; Antineoplastic agents ; Antineoplastic Agents - pharmacology ; Biological and medical sciences ; Blotting, Western ; Carcinoma, Pancreatic Ductal - pathology ; Cell Proliferation ; chemotherapy ; Drug Resistance, Neoplasm ; Female ; Gastroenterology. Liver. Pancreas. Abdomen ; Heme Oxygenase (Decyclizing) - biosynthesis ; Heme Oxygenase (Decyclizing) - genetics ; Heme Oxygenase (Decyclizing) - pharmacology ; Heme Oxygenase-1 ; Humans ; Liver. Biliary tract. Portal circulation. Exocrine pancreas ; Male ; Medical sciences ; Membrane Proteins ; Microscopy, Confocal ; Middle Aged ; pancreatic cancer ; Pancreatic Neoplasms - pathology ; Pharmacology. Drug treatments ; Polymerase Chain Reaction ; radiation ; Radiation Tolerance ; RNA, Messenger - analysis ; RNA, Messenger - biosynthesis ; Tumor Cells, Cultured ; Tumors ; Up-Regulation</subject><ispartof>Clinical cancer research, 2005-05, Vol.11 (10), p.3790-3798</ispartof><rights>2005 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-f3898f5bd42bb139a117c40f865100d318dce040ef992d4108facf9ff334a6d43</citedby><cites>FETCH-LOGICAL-c468t-f3898f5bd42bb139a117c40f865100d318dce040ef992d4108facf9ff334a6d43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3343,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16776128$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15897578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>BERBERAT, Pascal O</creatorcontrib><creatorcontrib>DAMBRAUSKAS, Zilvinas</creatorcontrib><creatorcontrib>GULBINAS, Antanas</creatorcontrib><creatorcontrib>GIESE, Thomas</creatorcontrib><creatorcontrib>GIESE, Nathalia</creatorcontrib><creatorcontrib>KÜNZLI, Beat</creatorcontrib><creatorcontrib>AUTSCHBACH, Frank</creatorcontrib><creatorcontrib>MEUER, Stefan</creatorcontrib><creatorcontrib>BÜCHLER, Markus W</creatorcontrib><creatorcontrib>FRIESS, Helmut</creatorcontrib><title>Inhibition of Heme Oxygenase-1 Increases Responsiveness of Pancreatic Cancer Cells to Anticancer Treatment</title><title>Clinical cancer research</title><addtitle>Clin Cancer Res</addtitle><description>Heme oxygenase-1 (HO-1) is believed to represent a key enzyme for the protection of cells against “stress.” Its overexpression
in different types of human cancers supports the notion that HO-1 provides a growth advantage and contributes to cellular
resistance against chemotherapy and radiotherapy. Given the poor survival rates of patients with pancreatic cancer due to
its aggressive growth behavior and its exceptional resistance to all known forms of anticancer treatment, we have investigated
the expression of HO-1 in human pancreatic cancer cells growth behavior and prognosis. Expression of HO-1 was analyzed in
human pancreatic cancer samples in comparison with normal pancreas by quantitative PCR, Western blot, and confocal microscopy.
The influence of radiotherapy and chemotherapy on HO-1 expression in pancreatic cancer cell lines was evaluated. Furthermore,
HO-1 expression was specifically suppressed by small interfering RNA transfection and subsequently the alterations of growth
behavior and resistance to anticancer treatment were tested. Human pancreatic cancer showed a 6-fold and 3.5-fold HO-1 up-regulation
in comparison to normal pancreas based on mRNA and protein level, respectively ( P < 0.05). Cancer tissues revealed marked HO-1 immunoreactivity in tumor cells and in tumor associated immunocytes. Treatment
of the pancreatic cancer cell lines with gemcitabine or radiation strongly induced HO-1 expression. Targeted knockdown of
HO-1 expression led to pronounced growth inhibition of the pancreatic cancer cells and made tumor cells significantly more
sensitive to radiotherapy and chemotherapy. Therefore, specific inhibition of HO-1 expression may be a new option in pancreatic
cancer therapy and may be used as sensitizer to chemotherapy and radiotherapy.</description><subject>Adult</subject><subject>Aged</subject><subject>anticancer therapy</subject><subject>Antineoplastic agents</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Cell Proliferation</subject><subject>chemotherapy</subject><subject>Drug Resistance, Neoplasm</subject><subject>Female</subject><subject>Gastroenterology. Liver. Pancreas. Abdomen</subject><subject>Heme Oxygenase (Decyclizing) - biosynthesis</subject><subject>Heme Oxygenase (Decyclizing) - genetics</subject><subject>Heme Oxygenase (Decyclizing) - pharmacology</subject><subject>Heme Oxygenase-1</subject><subject>Humans</subject><subject>Liver. Biliary tract. Portal circulation. Exocrine pancreas</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Proteins</subject><subject>Microscopy, Confocal</subject><subject>Middle Aged</subject><subject>pancreatic cancer</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Polymerase Chain Reaction</subject><subject>radiation</subject><subject>Radiation Tolerance</subject><subject>RNA, Messenger - analysis</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors</subject><subject>Up-Regulation</subject><issn>1078-0432</issn><issn>1557-3265</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU9v1DAQxS0Eon_gI4ByAamHFE9sJ86xioCuVKmoKmfLccZdVxtn8WSBfnscsqhHTn4a_2Y8fo-xd8AvAZT-BLzRJZeiuuy6uyzKClT7gp2CUk0pqlq9zPofc8LOiB45BwlcvmYneUDbqEafssdN3IY-zGGKxeSLaxyxuP399IDREpZQbKJLmCUVd0j7KVL4iRGJFvib_Xs5B1d0WWIqOtztqJin4irm6lq7X5AR4_yGvfJ2R_j2eJ6z718-33fX5c3t1013dVM6Weu59EK32qt-kFXfg2gtQOMk97pWwPkgQA8OueTo27Ya8oe0t8633gshbT1Icc4-rnP3afpxQJrNGMjlzWzE6UCmbnQeIqv_ghWArHgLGVQr6NJElNCbfQqjTU8GuFnSMIvTZnHa5DSyMEsaue_98YFDP-Lw3HW0PwMfjoAlZ3c-ZcsCPXN109RQLdzFym3Dw_ZXSGhWcxMS2uS2eYllFdG0XPwB_eyhCA</recordid><startdate>20050515</startdate><enddate>20050515</enddate><creator>BERBERAT, Pascal O</creator><creator>DAMBRAUSKAS, Zilvinas</creator><creator>GULBINAS, Antanas</creator><creator>GIESE, Thomas</creator><creator>GIESE, Nathalia</creator><creator>KÜNZLI, Beat</creator><creator>AUTSCHBACH, Frank</creator><creator>MEUER, Stefan</creator><creator>BÜCHLER, Markus W</creator><creator>FRIESS, Helmut</creator><general>American Association for Cancer Research</general><scope>IQODW</scope><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>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20050515</creationdate><title>Inhibition of Heme Oxygenase-1 Increases Responsiveness of Pancreatic Cancer Cells to Anticancer Treatment</title><author>BERBERAT, Pascal O ; DAMBRAUSKAS, Zilvinas ; GULBINAS, Antanas ; GIESE, Thomas ; GIESE, Nathalia ; KÜNZLI, Beat ; AUTSCHBACH, Frank ; MEUER, Stefan ; BÜCHLER, Markus W ; FRIESS, Helmut</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c468t-f3898f5bd42bb139a117c40f865100d318dce040ef992d4108facf9ff334a6d43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Adult</topic><topic>Aged</topic><topic>anticancer therapy</topic><topic>Antineoplastic agents</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Cell Proliferation</topic><topic>chemotherapy</topic><topic>Drug Resistance, Neoplasm</topic><topic>Female</topic><topic>Gastroenterology. Liver. Pancreas. Abdomen</topic><topic>Heme Oxygenase (Decyclizing) - biosynthesis</topic><topic>Heme Oxygenase (Decyclizing) - genetics</topic><topic>Heme Oxygenase (Decyclizing) - pharmacology</topic><topic>Heme Oxygenase-1</topic><topic>Humans</topic><topic>Liver. Biliary tract. Portal circulation. Exocrine pancreas</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Proteins</topic><topic>Microscopy, Confocal</topic><topic>Middle Aged</topic><topic>pancreatic cancer</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Polymerase Chain Reaction</topic><topic>radiation</topic><topic>Radiation Tolerance</topic><topic>RNA, Messenger - analysis</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>BERBERAT, Pascal O</creatorcontrib><creatorcontrib>DAMBRAUSKAS, Zilvinas</creatorcontrib><creatorcontrib>GULBINAS, Antanas</creatorcontrib><creatorcontrib>GIESE, Thomas</creatorcontrib><creatorcontrib>GIESE, Nathalia</creatorcontrib><creatorcontrib>KÜNZLI, Beat</creatorcontrib><creatorcontrib>AUTSCHBACH, Frank</creatorcontrib><creatorcontrib>MEUER, Stefan</creatorcontrib><creatorcontrib>BÜCHLER, Markus W</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><collection>CrossRef</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical cancer research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>BERBERAT, Pascal O</au><au>DAMBRAUSKAS, Zilvinas</au><au>GULBINAS, Antanas</au><au>GIESE, Thomas</au><au>GIESE, Nathalia</au><au>KÜNZLI, Beat</au><au>AUTSCHBACH, Frank</au><au>MEUER, Stefan</au><au>BÜCHLER, Markus W</au><au>FRIESS, Helmut</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of Heme Oxygenase-1 Increases Responsiveness of Pancreatic Cancer Cells to Anticancer Treatment</atitle><jtitle>Clinical cancer research</jtitle><addtitle>Clin Cancer Res</addtitle><date>2005-05-15</date><risdate>2005</risdate><volume>11</volume><issue>10</issue><spage>3790</spage><epage>3798</epage><pages>3790-3798</pages><issn>1078-0432</issn><eissn>1557-3265</eissn><abstract>Heme oxygenase-1 (HO-1) is believed to represent a key enzyme for the protection of cells against “stress.” Its overexpression
in different types of human cancers supports the notion that HO-1 provides a growth advantage and contributes to cellular
resistance against chemotherapy and radiotherapy. Given the poor survival rates of patients with pancreatic cancer due to
its aggressive growth behavior and its exceptional resistance to all known forms of anticancer treatment, we have investigated
the expression of HO-1 in human pancreatic cancer cells growth behavior and prognosis. Expression of HO-1 was analyzed in
human pancreatic cancer samples in comparison with normal pancreas by quantitative PCR, Western blot, and confocal microscopy.
The influence of radiotherapy and chemotherapy on HO-1 expression in pancreatic cancer cell lines was evaluated. Furthermore,
HO-1 expression was specifically suppressed by small interfering RNA transfection and subsequently the alterations of growth
behavior and resistance to anticancer treatment were tested. Human pancreatic cancer showed a 6-fold and 3.5-fold HO-1 up-regulation
in comparison to normal pancreas based on mRNA and protein level, respectively ( P < 0.05). Cancer tissues revealed marked HO-1 immunoreactivity in tumor cells and in tumor associated immunocytes. Treatment
of the pancreatic cancer cell lines with gemcitabine or radiation strongly induced HO-1 expression. Targeted knockdown of
HO-1 expression led to pronounced growth inhibition of the pancreatic cancer cells and made tumor cells significantly more
sensitive to radiotherapy and chemotherapy. Therefore, specific inhibition of HO-1 expression may be a new option in pancreatic
cancer therapy and may be used as sensitizer to chemotherapy and radiotherapy.</abstract><cop>Philadelphia, PA</cop><pub>American Association for Cancer Research</pub><pmid>15897578</pmid><doi>10.1158/1078-0432.CCR-04-2159</doi><tpages>9</tpages></addata></record> |
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| ispartof | Clinical cancer research, 2005-05, Vol.11 (10), p.3790-3798 |
| issn | 1078-0432 1557-3265 |
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| source | MEDLINE; American Association for Cancer Research; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Adult Aged anticancer therapy Antineoplastic agents Antineoplastic Agents - pharmacology Biological and medical sciences Blotting, Western Carcinoma, Pancreatic Ductal - pathology Cell Proliferation chemotherapy Drug Resistance, Neoplasm Female Gastroenterology. Liver. Pancreas. Abdomen Heme Oxygenase (Decyclizing) - biosynthesis Heme Oxygenase (Decyclizing) - genetics Heme Oxygenase (Decyclizing) - pharmacology Heme Oxygenase-1 Humans Liver. Biliary tract. Portal circulation. Exocrine pancreas Male Medical sciences Membrane Proteins Microscopy, Confocal Middle Aged pancreatic cancer Pancreatic Neoplasms - pathology Pharmacology. Drug treatments Polymerase Chain Reaction radiation Radiation Tolerance RNA, Messenger - analysis RNA, Messenger - biosynthesis Tumor Cells, Cultured Tumors Up-Regulation |
| title | Inhibition of Heme Oxygenase-1 Increases Responsiveness of Pancreatic Cancer Cells to Anticancer Treatment |
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