A feasibility study on gene therapy of pancreatic carcinoma with Ad-PUMA
Pancreatic cancer is one of the most malignant tumors with high mortality and poor prognosis even with the aggressive conventional therapies. Biotherapy based on the understanding of tumorigenesis mechanism is ongoing to improve the outcomes of cancer patients. We sought here to evaluate the therape...
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| Veröffentlicht in: | Cancer biology & therapy 2012-07, Vol.13 (9), p.712-719 |
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| creator | Wang, Haijuan Pei, Wei Luan, Qingchun Ma, Fei Zhou, Shaohua zhao, zhilong Meng, Xiting Zhang, Xueyan Liang, Xiao Chen, Yan Zhan, Qimin Lin, Chen Qian, Haili Zhao, Ping |
| description | Pancreatic cancer is one of the most malignant tumors with high mortality and poor prognosis even with the aggressive conventional therapies. Biotherapy based on the understanding of tumorigenesis mechanism is ongoing to improve the outcomes of cancer patients. We sought here to evaluate the therapeutic potential of a proapoptotic gene, PUMA, in pancreatic cancer. We found that PUMA was differently expressed in a series of pancreatic ductal adenocarcinoma cancer cell lines, and adenovirus-mediated expression of PUMA (Ad-PUMA) in these cells resulted in massive apoptosis. PUMA was more potent than p53 in suppressing growth of cancer cells. RT-PCR and Western Blot revealed that exogenous PUMA was expressed 6 h after Ad-PUMA infection. Furthermore, we assessed the efficacy of Ad-PUMA combining anticancer drugs (5-fluorouracil, cisplatin, gemcitabine hydrochloride, respectively) in these pancreatic cancer cell lines. Data revealed that PUMA significantly sensitized pancreatic carcinoma cell lines to chemotherapeutics, which may be resulted from abundant apoptosis induction. In nude mice with PANC-1 xenografts, Ad-PUMA treatment significantly inhibited the tumor growth. These results suggest that PUMA is a potent molecular tool in suppressing tumor growth sensitizing pancreatic carcinoma cells to chemical drugs. PUMA plays roles in negatively regulating cancer cell growth and may be a promising tool for cancer biotherapy, with or without combination with chemotherapeutic agents. |
| doi_str_mv | 10.4161/cbt.20552 |
| format | Article |
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Biotherapy based on the understanding of tumorigenesis mechanism is ongoing to improve the outcomes of cancer patients. We sought here to evaluate the therapeutic potential of a proapoptotic gene, PUMA, in pancreatic cancer. We found that PUMA was differently expressed in a series of pancreatic ductal adenocarcinoma cancer cell lines, and adenovirus-mediated expression of PUMA (Ad-PUMA) in these cells resulted in massive apoptosis. PUMA was more potent than p53 in suppressing growth of cancer cells. RT-PCR and Western Blot revealed that exogenous PUMA was expressed 6 h after Ad-PUMA infection. Furthermore, we assessed the efficacy of Ad-PUMA combining anticancer drugs (5-fluorouracil, cisplatin, gemcitabine hydrochloride, respectively) in these pancreatic cancer cell lines. Data revealed that PUMA significantly sensitized pancreatic carcinoma cell lines to chemotherapeutics, which may be resulted from abundant apoptosis induction. In nude mice with PANC-1 xenografts, Ad-PUMA treatment significantly inhibited the tumor growth. These results suggest that PUMA is a potent molecular tool in suppressing tumor growth sensitizing pancreatic carcinoma cells to chemical drugs. PUMA plays roles in negatively regulating cancer cell growth and may be a promising tool for cancer biotherapy, with or without combination with chemotherapeutic agents.</description><identifier>ISSN: 1538-4047</identifier><identifier>EISSN: 1555-8576</identifier><identifier>DOI: 10.4161/cbt.20552</identifier><identifier>PMID: 22617775</identifier><language>eng</language><publisher>United States: Taylor & Francis</publisher><subject>Adenoviridae - genetics ; adenovirus ; Animals ; Antineoplastic Agents - pharmacology ; Apoptosis ; Apoptosis Regulatory Proteins - biosynthesis ; Apoptosis Regulatory Proteins - genetics ; Binding ; Biology ; Bioscience ; Calcium ; Cancer ; Carcinoma, Pancreatic Ductal - pathology ; Carcinoma, Pancreatic Ductal - therapy ; Cell ; Cell Line, Tumor ; Cell Proliferation ; Cell Survival ; Cisplatin - pharmacology ; Combined Modality Therapy ; Cycle ; Deoxycytidine - analogs & derivatives ; Deoxycytidine - pharmacology ; Feasibility Studies ; Fluorouracil - pharmacology ; Gene Expression ; gene therapy ; Genetic Therapy ; Genetic Vectors ; Humans ; Inhibitory Concentration 50 ; Landes ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Organogenesis ; pancreatic cancer ; Pancreatic Neoplasms - pathology ; Pancreatic Neoplasms - therapy ; Proteins ; Proto-Oncogene Proteins - biosynthesis ; Proto-Oncogene Proteins - genetics ; PUMA ; Tumor Burden ; Tumor Suppressor Protein p53 - biosynthesis ; Tumor Suppressor Protein p53 - genetics</subject><ispartof>Cancer biology & therapy, 2012-07, Vol.13 (9), p.712-719</ispartof><rights>Copyright © 2012 Landes Bioscience 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c563t-40eed557f3067948703142f012d356f21cb32bcd3a91268ccf8abe4bdd89ad663</citedby><cites>FETCH-LOGICAL-c563t-40eed557f3067948703142f012d356f21cb32bcd3a91268ccf8abe4bdd89ad663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22617775$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Haijuan</creatorcontrib><creatorcontrib>Pei, Wei</creatorcontrib><creatorcontrib>Luan, Qingchun</creatorcontrib><creatorcontrib>Ma, Fei</creatorcontrib><creatorcontrib>Zhou, Shaohua</creatorcontrib><creatorcontrib>zhao, zhilong</creatorcontrib><creatorcontrib>Meng, Xiting</creatorcontrib><creatorcontrib>Zhang, Xueyan</creatorcontrib><creatorcontrib>Liang, Xiao</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Zhan, Qimin</creatorcontrib><creatorcontrib>Lin, Chen</creatorcontrib><creatorcontrib>Qian, Haili</creatorcontrib><creatorcontrib>Zhao, Ping</creatorcontrib><title>A feasibility study on gene therapy of pancreatic carcinoma with Ad-PUMA</title><title>Cancer biology & therapy</title><addtitle>Cancer Biol Ther</addtitle><description>Pancreatic cancer is one of the most malignant tumors with high mortality and poor prognosis even with the aggressive conventional therapies. Biotherapy based on the understanding of tumorigenesis mechanism is ongoing to improve the outcomes of cancer patients. We sought here to evaluate the therapeutic potential of a proapoptotic gene, PUMA, in pancreatic cancer. We found that PUMA was differently expressed in a series of pancreatic ductal adenocarcinoma cancer cell lines, and adenovirus-mediated expression of PUMA (Ad-PUMA) in these cells resulted in massive apoptosis. PUMA was more potent than p53 in suppressing growth of cancer cells. RT-PCR and Western Blot revealed that exogenous PUMA was expressed 6 h after Ad-PUMA infection. Furthermore, we assessed the efficacy of Ad-PUMA combining anticancer drugs (5-fluorouracil, cisplatin, gemcitabine hydrochloride, respectively) in these pancreatic cancer cell lines. Data revealed that PUMA significantly sensitized pancreatic carcinoma cell lines to chemotherapeutics, which may be resulted from abundant apoptosis induction. In nude mice with PANC-1 xenografts, Ad-PUMA treatment significantly inhibited the tumor growth. These results suggest that PUMA is a potent molecular tool in suppressing tumor growth sensitizing pancreatic carcinoma cells to chemical drugs. PUMA plays roles in negatively regulating cancer cell growth and may be a promising tool for cancer biotherapy, with or without combination with chemotherapeutic agents.</description><subject>Adenoviridae - genetics</subject><subject>adenovirus</subject><subject>Animals</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - biosynthesis</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Binding</subject><subject>Biology</subject><subject>Bioscience</subject><subject>Calcium</subject><subject>Cancer</subject><subject>Carcinoma, Pancreatic Ductal - pathology</subject><subject>Carcinoma, Pancreatic Ductal - therapy</subject><subject>Cell</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Cell Survival</subject><subject>Cisplatin - pharmacology</subject><subject>Combined Modality Therapy</subject><subject>Cycle</subject><subject>Deoxycytidine - analogs & derivatives</subject><subject>Deoxycytidine - pharmacology</subject><subject>Feasibility Studies</subject><subject>Fluorouracil - pharmacology</subject><subject>Gene Expression</subject><subject>gene therapy</subject><subject>Genetic Therapy</subject><subject>Genetic Vectors</subject><subject>Humans</subject><subject>Inhibitory Concentration 50</subject><subject>Landes</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Neoplasm Transplantation</subject><subject>Organogenesis</subject><subject>pancreatic cancer</subject><subject>Pancreatic Neoplasms - pathology</subject><subject>Pancreatic Neoplasms - therapy</subject><subject>Proteins</subject><subject>Proto-Oncogene Proteins - biosynthesis</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>PUMA</subject><subject>Tumor Burden</subject><subject>Tumor Suppressor Protein p53 - biosynthesis</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><issn>1538-4047</issn><issn>1555-8576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqdks1u1DAUhS0Eoj90wQsgL2GR4p_YSZbDqDBIRe2iFd1Zjn3dGiVxsD2q5u3xNG0lxALByrb0fedeHRmht5Sc1lTSj6bPp4wIwV6gQyqEqFrRyJf7O2-rmtTNATpK6QchrGGye40OGJO0aRpxiDYr7EAn3_vB5x1OeWt3OEz4FibA-Q6insvb4VlPJoLO3mCjo_FTGDW-9_kOr2x1ef1t9Qa9cnpIcPJ4HqPrz2dX6011fvHl63p1XhkheS7bAFghGseJbLq6bQinNXOEMsuFdIyanrPeWK47ymRrjGt1D3VvbdtpKyU_Ru-X3DmGn1tIWY0-GRgGPUHYJkWJ7BipWy4K-mFBTQwpRXBqjn7UcVcgtS9OleLUQ3GFffcYu-1HsM_kU1MF6BagDLKQeh-S8TAZeEb3YTqWhgZYQp_GFHf9v-5vK9J_TSmO-ItDuNp819Pt-tMV5apTN2q2rnj14vnJhTjq-xAHq7LeDSG6WP6CT4r_ueIvpLvKIw</recordid><startdate>20120701</startdate><enddate>20120701</enddate><creator>Wang, Haijuan</creator><creator>Pei, Wei</creator><creator>Luan, Qingchun</creator><creator>Ma, Fei</creator><creator>Zhou, Shaohua</creator><creator>zhao, zhilong</creator><creator>Meng, Xiting</creator><creator>Zhang, Xueyan</creator><creator>Liang, Xiao</creator><creator>Chen, Yan</creator><creator>Zhan, Qimin</creator><creator>Lin, Chen</creator><creator>Qian, Haili</creator><creator>Zhao, Ping</creator><general>Taylor & Francis</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></search><sort><creationdate>20120701</creationdate><title>A feasibility study on gene therapy of pancreatic carcinoma with Ad-PUMA</title><author>Wang, Haijuan ; Pei, Wei ; Luan, Qingchun ; Ma, Fei ; Zhou, Shaohua ; zhao, zhilong ; Meng, Xiting ; Zhang, Xueyan ; Liang, Xiao ; Chen, Yan ; Zhan, Qimin ; Lin, Chen ; Qian, Haili ; Zhao, Ping</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c563t-40eed557f3067948703142f012d356f21cb32bcd3a91268ccf8abe4bdd89ad663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenoviridae - genetics</topic><topic>adenovirus</topic><topic>Animals</topic><topic>Antineoplastic Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - biosynthesis</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Binding</topic><topic>Biology</topic><topic>Bioscience</topic><topic>Calcium</topic><topic>Cancer</topic><topic>Carcinoma, Pancreatic Ductal - pathology</topic><topic>Carcinoma, Pancreatic Ductal - therapy</topic><topic>Cell</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Cell Survival</topic><topic>Cisplatin - pharmacology</topic><topic>Combined Modality Therapy</topic><topic>Cycle</topic><topic>Deoxycytidine - analogs & derivatives</topic><topic>Deoxycytidine - pharmacology</topic><topic>Feasibility Studies</topic><topic>Fluorouracil - pharmacology</topic><topic>Gene Expression</topic><topic>gene therapy</topic><topic>Genetic Therapy</topic><topic>Genetic Vectors</topic><topic>Humans</topic><topic>Inhibitory Concentration 50</topic><topic>Landes</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Neoplasm Transplantation</topic><topic>Organogenesis</topic><topic>pancreatic cancer</topic><topic>Pancreatic Neoplasms - pathology</topic><topic>Pancreatic Neoplasms - therapy</topic><topic>Proteins</topic><topic>Proto-Oncogene Proteins - biosynthesis</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>PUMA</topic><topic>Tumor Burden</topic><topic>Tumor Suppressor Protein p53 - biosynthesis</topic><topic>Tumor Suppressor Protein p53 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Haijuan</creatorcontrib><creatorcontrib>Pei, Wei</creatorcontrib><creatorcontrib>Luan, Qingchun</creatorcontrib><creatorcontrib>Ma, Fei</creatorcontrib><creatorcontrib>Zhou, Shaohua</creatorcontrib><creatorcontrib>zhao, zhilong</creatorcontrib><creatorcontrib>Meng, Xiting</creatorcontrib><creatorcontrib>Zhang, Xueyan</creatorcontrib><creatorcontrib>Liang, Xiao</creatorcontrib><creatorcontrib>Chen, Yan</creatorcontrib><creatorcontrib>Zhan, Qimin</creatorcontrib><creatorcontrib>Lin, Chen</creatorcontrib><creatorcontrib>Qian, Haili</creatorcontrib><creatorcontrib>Zhao, Ping</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><jtitle>Cancer biology & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Haijuan</au><au>Pei, Wei</au><au>Luan, Qingchun</au><au>Ma, Fei</au><au>Zhou, Shaohua</au><au>zhao, zhilong</au><au>Meng, Xiting</au><au>Zhang, Xueyan</au><au>Liang, Xiao</au><au>Chen, Yan</au><au>Zhan, Qimin</au><au>Lin, Chen</au><au>Qian, Haili</au><au>Zhao, Ping</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A feasibility study on gene therapy of pancreatic carcinoma with Ad-PUMA</atitle><jtitle>Cancer biology & therapy</jtitle><addtitle>Cancer Biol Ther</addtitle><date>2012-07-01</date><risdate>2012</risdate><volume>13</volume><issue>9</issue><spage>712</spage><epage>719</epage><pages>712-719</pages><issn>1538-4047</issn><eissn>1555-8576</eissn><abstract>Pancreatic cancer is one of the most malignant tumors with high mortality and poor prognosis even with the aggressive conventional therapies. Biotherapy based on the understanding of tumorigenesis mechanism is ongoing to improve the outcomes of cancer patients. We sought here to evaluate the therapeutic potential of a proapoptotic gene, PUMA, in pancreatic cancer. We found that PUMA was differently expressed in a series of pancreatic ductal adenocarcinoma cancer cell lines, and adenovirus-mediated expression of PUMA (Ad-PUMA) in these cells resulted in massive apoptosis. PUMA was more potent than p53 in suppressing growth of cancer cells. RT-PCR and Western Blot revealed that exogenous PUMA was expressed 6 h after Ad-PUMA infection. Furthermore, we assessed the efficacy of Ad-PUMA combining anticancer drugs (5-fluorouracil, cisplatin, gemcitabine hydrochloride, respectively) in these pancreatic cancer cell lines. Data revealed that PUMA significantly sensitized pancreatic carcinoma cell lines to chemotherapeutics, which may be resulted from abundant apoptosis induction. In nude mice with PANC-1 xenografts, Ad-PUMA treatment significantly inhibited the tumor growth. These results suggest that PUMA is a potent molecular tool in suppressing tumor growth sensitizing pancreatic carcinoma cells to chemical drugs. PUMA plays roles in negatively regulating cancer cell growth and may be a promising tool for cancer biotherapy, with or without combination with chemotherapeutic agents.</abstract><cop>United States</cop><pub>Taylor & Francis</pub><pmid>22617775</pmid><doi>10.4161/cbt.20552</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cancer biology & therapy, 2012-07, Vol.13 (9), p.712-719 |
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| subjects | Adenoviridae - genetics adenovirus Animals Antineoplastic Agents - pharmacology Apoptosis Apoptosis Regulatory Proteins - biosynthesis Apoptosis Regulatory Proteins - genetics Binding Biology Bioscience Calcium Cancer Carcinoma, Pancreatic Ductal - pathology Carcinoma, Pancreatic Ductal - therapy Cell Cell Line, Tumor Cell Proliferation Cell Survival Cisplatin - pharmacology Combined Modality Therapy Cycle Deoxycytidine - analogs & derivatives Deoxycytidine - pharmacology Feasibility Studies Fluorouracil - pharmacology Gene Expression gene therapy Genetic Therapy Genetic Vectors Humans Inhibitory Concentration 50 Landes Mice Mice, Nude Neoplasm Transplantation Organogenesis pancreatic cancer Pancreatic Neoplasms - pathology Pancreatic Neoplasms - therapy Proteins Proto-Oncogene Proteins - biosynthesis Proto-Oncogene Proteins - genetics PUMA Tumor Burden Tumor Suppressor Protein p53 - biosynthesis Tumor Suppressor Protein p53 - genetics |
| title | A feasibility study on gene therapy of pancreatic carcinoma with Ad-PUMA |
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