5-aza-2′-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells
Treating lung cancer cell lines using low-dose 5-aza-2′-deoxycytidine (DAC) caused an accumulation of procaspase-9 through mRNA upregulation, but the cells did not undergo apoptosis. However, when cells were treated with DAC and infected with a low dose of a recombinant wild-type p53 adenovirus vect...
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| Veröffentlicht in: | Oncogene 2004-09, Vol.23 (40), p.6779-6787 |
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| creator | Gomyo, Yoshihito Sasaki, Ji-ichiro Branch, Cynthia Roth, Jack A Mukhopadhyay, Tapas |
| description | Treating lung cancer cell lines using low-dose 5-aza-2′-deoxycytidine (DAC) caused an accumulation of procaspase-9 through mRNA upregulation, but the cells did not undergo apoptosis. However, when cells were treated with DAC and infected with a low dose of a recombinant wild-type p53 adenovirus vector (Ad-p53), a synergistic growth inhibitory effect was observed. Combination treatment induced Apaf-1 and procaspase-9 expression in which cytochrome
c
releases by Ad-p53 triggered the mitochondrial pathway of apoptosis. Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells. In addition, DAC sensitized lung cancer cells to cisplatin and paclitaxel. Induction of the mitochondrial pathway of apoptosis using a slightly toxic dose of DAC may therefore be a strategy for treating lung cancer, and DAC treatment may have clinical implications when combined with chemotherapy or apoptosis-inducing gene therapy. |
| doi_str_mv | 10.1038/sj.onc.1207381 |
| format | Article |
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releases by Ad-p53 triggered the mitochondrial pathway of apoptosis. Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells. In addition, DAC sensitized lung cancer cells to cisplatin and paclitaxel. Induction of the mitochondrial pathway of apoptosis using a slightly toxic dose of DAC may therefore be a strategy for treating lung cancer, and DAC treatment may have clinical implications when combined with chemotherapy or apoptosis-inducing gene therapy.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1207381</identifier><identifier>PMID: 15273730</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Adenovirus ; Ageing, cell death ; Antimetabolites, Antineoplastic - pharmacology ; Apaf-1 protein ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - physiology ; Azacitidine - analogs & derivatives ; Azacitidine - pharmacology ; Biological and medical sciences ; Cancer therapies ; Caspase 9 ; Caspases - genetics ; Cell Biology ; Cell Line, Tumor ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Chemotherapy ; Cisplatin ; Cytochrome c ; Fundamental and applied biological sciences. Psychology ; Gene Expression Regulation, Enzymologic - drug effects ; Gene Expression Regulation, Enzymologic - genetics ; Gene Expression Regulation, Neoplastic - drug effects ; Gene Expression Regulation, Neoplastic - genetics ; Gene therapy ; Human Genetics ; Humans ; Internal Medicine ; Lung cancer ; Lung Neoplasms - pathology ; Medical sciences ; Medicine ; Medicine & Public Health ; Mitochondria ; Molecular and cellular biology ; mRNA ; Null cells ; Oncology ; original-paper ; p53 Protein ; Paclitaxel ; Pneumology ; Tumor cell lines ; Tumor Suppressor Protein p53 - physiology ; Tumors of the respiratory system and mediastinum</subject><ispartof>Oncogene, 2004-09, Vol.23 (40), p.6779-6787</ispartof><rights>Springer Nature Limited 2004</rights><rights>2004 INIST-CNRS</rights><rights>COPYRIGHT 2004 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Sep 2, 2004</rights><rights>Nature Publishing Group 2004.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c514t-8005d5aef8b6ae4a0f7c490f995e11a49e7b45b63dbae9c70ca4d1e15275abd73</citedby><cites>FETCH-LOGICAL-c514t-8005d5aef8b6ae4a0f7c490f995e11a49e7b45b63dbae9c70ca4d1e15275abd73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1207381$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1207381$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16101000$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15273730$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Gomyo, Yoshihito</creatorcontrib><creatorcontrib>Sasaki, Ji-ichiro</creatorcontrib><creatorcontrib>Branch, Cynthia</creatorcontrib><creatorcontrib>Roth, Jack A</creatorcontrib><creatorcontrib>Mukhopadhyay, Tapas</creatorcontrib><title>5-aza-2′-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>Treating lung cancer cell lines using low-dose 5-aza-2′-deoxycytidine (DAC) caused an accumulation of procaspase-9 through mRNA upregulation, but the cells did not undergo apoptosis. However, when cells were treated with DAC and infected with a low dose of a recombinant wild-type p53 adenovirus vector (Ad-p53), a synergistic growth inhibitory effect was observed. Combination treatment induced Apaf-1 and procaspase-9 expression in which cytochrome
c
releases by Ad-p53 triggered the mitochondrial pathway of apoptosis. Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells. In addition, DAC sensitized lung cancer cells to cisplatin and paclitaxel. Induction of the mitochondrial pathway of apoptosis using a slightly toxic dose of DAC may therefore be a strategy for treating lung cancer, and DAC treatment may have clinical implications when combined with chemotherapy or apoptosis-inducing gene therapy.</description><subject>Adenovirus</subject><subject>Ageing, cell death</subject><subject>Antimetabolites, Antineoplastic - pharmacology</subject><subject>Apaf-1 protein</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - physiology</subject><subject>Azacitidine - analogs & derivatives</subject><subject>Azacitidine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Cancer therapies</subject><subject>Caspase 9</subject><subject>Caspases - genetics</subject><subject>Cell Biology</subject><subject>Cell Line, Tumor</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Chemotherapy</subject><subject>Cisplatin</subject><subject>Cytochrome c</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gene Expression Regulation, Enzymologic - drug effects</subject><subject>Gene Expression Regulation, Enzymologic - genetics</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Gene Expression Regulation, Neoplastic - genetics</subject><subject>Gene therapy</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Lung cancer</subject><subject>Lung Neoplasms - pathology</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mitochondria</subject><subject>Molecular and cellular biology</subject><subject>mRNA</subject><subject>Null cells</subject><subject>Oncology</subject><subject>original-paper</subject><subject>p53 Protein</subject><subject>Paclitaxel</subject><subject>Pneumology</subject><subject>Tumor cell lines</subject><subject>Tumor Suppressor Protein p53 - physiology</subject><subject>Tumors of the respiratory system and mediastinum</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</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>eNp1ks9u1DAQxiMEokvhyhFZILhlayd2Eh-rin9SJS5wtibOZOtVYgdPIrpw4Zl4JJ4ErxppJdTKB0szv5n5xv6y7KXgW8HL5oL22-DtVhS8LhvxKNsIWVe5Ulo-zjZcK57roizOsmdEe855rXnxNDsTqqjLuuSb7JfK4Sfkxd_ff_IOw-3BHmbXOY9smSLulgFmJGaBJiDMNcPbFCZywTMbwoQRZud37Iebb9ikytz5brHYMZjCNAdyxJxnN8sIng1LAi14i5FZHAZ6nj3pYSB8sd7n2bcP779efcqvv3z8fHV5nVsl5Jw3nKtOAfZNWwFK4H1tpea91gqFAKmxbqVqq7JrAbWtuQXZCTzuqKDt6vI8e3fXd4rh-4I0m9HRUQF4DAsZUVe6aRqdwDf_gfuwRJ-0maKSoiybQhSJev0glZ5Vat3IU6sdDGic78McwR7nmkvRaK61LqpEbe-h0ulwdDZ47F2K31dgYyCK2JspuhHiwQhujoYwtDfJEGY1RCp4tYpd2hG7E746IAFvVwDIwtDH9EGOTlwluEjGSdzFHUcp5XcYT1s_MPofWIzO0g</recordid><startdate>20040902</startdate><enddate>20040902</enddate><creator>Gomyo, Yoshihito</creator><creator>Sasaki, Ji-ichiro</creator><creator>Branch, Cynthia</creator><creator>Roth, Jack A</creator><creator>Mukhopadhyay, Tapas</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</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>3V.</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>FR3</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>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope></search><sort><creationdate>20040902</creationdate><title>5-aza-2′-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells</title><author>Gomyo, Yoshihito ; Sasaki, Ji-ichiro ; Branch, Cynthia ; Roth, Jack A ; Mukhopadhyay, Tapas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c514t-8005d5aef8b6ae4a0f7c490f995e11a49e7b45b63dbae9c70ca4d1e15275abd73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adenovirus</topic><topic>Ageing, cell death</topic><topic>Antimetabolites, Antineoplastic - pharmacology</topic><topic>Apaf-1 protein</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - physiology</topic><topic>Azacitidine - analogs & derivatives</topic><topic>Azacitidine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Cancer therapies</topic><topic>Caspase 9</topic><topic>Caspases - genetics</topic><topic>Cell Biology</topic><topic>Cell Line, Tumor</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. 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One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gomyo, Yoshihito</au><au>Sasaki, Ji-ichiro</au><au>Branch, Cynthia</au><au>Roth, Jack A</au><au>Mukhopadhyay, Tapas</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>5-aza-2′-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2004-09-02</date><risdate>2004</risdate><volume>23</volume><issue>40</issue><spage>6779</spage><epage>6787</epage><pages>6779-6787</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>Treating lung cancer cell lines using low-dose 5-aza-2′-deoxycytidine (DAC) caused an accumulation of procaspase-9 through mRNA upregulation, but the cells did not undergo apoptosis. However, when cells were treated with DAC and infected with a low dose of a recombinant wild-type p53 adenovirus vector (Ad-p53), a synergistic growth inhibitory effect was observed. Combination treatment induced Apaf-1 and procaspase-9 expression in which cytochrome
c
releases by Ad-p53 triggered the mitochondrial pathway of apoptosis. Selective blockage of caspase-9 activities by Z-LEHD-FMK completely attenuated DAC-induced enhancement of apoptosis mediated by Ad-p53 infection, and ectopic overexpression of procaspase-9 sensitized cells to Ad-p53-induced apoptosis in p53-null cells. In addition, DAC sensitized lung cancer cells to cisplatin and paclitaxel. Induction of the mitochondrial pathway of apoptosis using a slightly toxic dose of DAC may therefore be a strategy for treating lung cancer, and DAC treatment may have clinical implications when combined with chemotherapy or apoptosis-inducing gene therapy.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>15273730</pmid><doi>10.1038/sj.onc.1207381</doi><tpages>9</tpages></addata></record> |
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| subjects | Adenovirus Ageing, cell death Antimetabolites, Antineoplastic - pharmacology Apaf-1 protein Apoptosis Apoptosis - drug effects Apoptosis - physiology Azacitidine - analogs & derivatives Azacitidine - pharmacology Biological and medical sciences Cancer therapies Caspase 9 Caspases - genetics Cell Biology Cell Line, Tumor Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Chemotherapy Cisplatin Cytochrome c Fundamental and applied biological sciences. Psychology Gene Expression Regulation, Enzymologic - drug effects Gene Expression Regulation, Enzymologic - genetics Gene Expression Regulation, Neoplastic - drug effects Gene Expression Regulation, Neoplastic - genetics Gene therapy Human Genetics Humans Internal Medicine Lung cancer Lung Neoplasms - pathology Medical sciences Medicine Medicine & Public Health Mitochondria Molecular and cellular biology mRNA Null cells Oncology original-paper p53 Protein Paclitaxel Pneumology Tumor cell lines Tumor Suppressor Protein p53 - physiology Tumors of the respiratory system and mediastinum |
| title | 5-aza-2′-deoxycytidine upregulates caspase-9 expression cooperating with p53-induced apoptosis in human lung cancer cells |
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