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Suppression of Bcl-xL expression by a novel tumor-specific RNA interference system inhibits proliferation and enhances radiosensitivity in prostatic carcinoma cells
Bcl-xL , a novel member of anti-apoptotic Bcl-2 family that play important roles in regulating cell survival and apoptosis, is frequently overexpressed in various kinds of human cancers, including prostatic carcinoma. To explore its possibility as a therapeutic target for prostatic carcinoma, we dev...
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| Published in: | Cancer chemotherapy and pharmacology 2008-05, Vol.61 (6), p.943-952 |
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| container_end_page | 952 |
| container_issue | 6 |
| container_start_page | 943 |
| container_title | Cancer chemotherapy and pharmacology |
| container_volume | 61 |
| creator | Wang, Rui Lin, Fang Wang, Xi Gao, Ping Dong, Ke Wei, San-Hua Cheng, Shi-Yin Zhang, Hui-Zhong |
| description | Bcl-xL
, a novel member of anti-apoptotic
Bcl-2
family that play important roles in regulating cell survival and apoptosis, is frequently overexpressed in various kinds of human cancers, including prostatic carcinoma. To explore its possibility as a therapeutic target for prostatic carcinoma, we developed a novel tumor-specific RNA interference system by using survivin promoter and employed it to suppress exogenous reporters (
LUC
and
EGFP
) and endogenous gene
Bcl-xL
expression and analyzed its phenotypes. We found that expression of exogenous reporters (
LUC
and
EGFP
) was specifically inhibited in tumor cells but not in normal cells. We also observed that the specific inhibition of
Bcl-xL
in human prostatic carcinoma cells (PC3) strongly suppressed in vitro cell proliferation and in vivo tumorigenicity. We observed significant apoptosis induction and radiosensitivity enhancement in PC3 cells by the RNA interference-mediated suppression of
Bcl-xL
expression. All these results indicate that inhibition of
Bcl-xL
expression can result in potent antitumor activity and radiosensitization in human prostatic carcinoma. |
| doi_str_mv | 10.1007/s00280-007-0548-y |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_68090883</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1453048061</sourcerecordid><originalsourceid>FETCH-LOGICAL-c496t-6336cabddc2014f775dd7e665be47ad61655465bec3cfaca691f57f42875c5d73</originalsourceid><addsrcrecordid>eNqFkctu1TAQhi0EoqeFB2CDLCTYGcbxLVm2FRSkI5C4rCPHcairxAmepGrehwfF0TlqJSTEyuOZb36P5yfkBYe3HMC8Q4CiBJZDBkqWbH1EdlyKgkEpxWOyAyElUwbkCTlFvAEAyYV4Sk640UoYbnbk97dlmpJHDGOkY0cvXM_u9tTf3SeblVoax1vf03kZxsRw8i50wdGvn89piLNPnU8-Ok9xxdkPOXcdmjAjndLYh1y08yZkY0t9vLaZRJpsG0b0EcMcbsO85qYNxzmzjjqbXIjjYKnzfY_PyJPO9uifH88z8uPD---XH9n-y9Wny_M9c7LSM9NCaGebtnUFcNkZo9rWeK1V46WxreZaKbndnHCddVZXvFOmk0VplFOtEWfkzUE3T_Jr8TjXQ8BtAhv9uGCtS6igLMV_QV7pSpgKMvjqL_BmXFLMn6gLLqQxhZYZ4gfI5QVg8l09pTDYtNYc6s3o-mB0vYWb0fWae14ehZdm8O1Dx9HZDLw-Ahad7buU9x7wniugAKjkxhUHDnMp_vTpYcJ_v_4H4PnE2w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>213477264</pqid></control><display><type>article</type><title>Suppression of Bcl-xL expression by a novel tumor-specific RNA interference system inhibits proliferation and enhances radiosensitivity in prostatic carcinoma cells</title><source>Springer Nature</source><creator>Wang, Rui ; Lin, Fang ; Wang, Xi ; Gao, Ping ; Dong, Ke ; Wei, San-Hua ; Cheng, Shi-Yin ; Zhang, Hui-Zhong</creator><creatorcontrib>Wang, Rui ; Lin, Fang ; Wang, Xi ; Gao, Ping ; Dong, Ke ; Wei, San-Hua ; Cheng, Shi-Yin ; Zhang, Hui-Zhong</creatorcontrib><description>Bcl-xL
, a novel member of anti-apoptotic
Bcl-2
family that play important roles in regulating cell survival and apoptosis, is frequently overexpressed in various kinds of human cancers, including prostatic carcinoma. To explore its possibility as a therapeutic target for prostatic carcinoma, we developed a novel tumor-specific RNA interference system by using survivin promoter and employed it to suppress exogenous reporters (
LUC
and
EGFP
) and endogenous gene
Bcl-xL
expression and analyzed its phenotypes. We found that expression of exogenous reporters (
LUC
and
EGFP
) was specifically inhibited in tumor cells but not in normal cells. We also observed that the specific inhibition of
Bcl-xL
in human prostatic carcinoma cells (PC3) strongly suppressed in vitro cell proliferation and in vivo tumorigenicity. We observed significant apoptosis induction and radiosensitivity enhancement in PC3 cells by the RNA interference-mediated suppression of
Bcl-xL
expression. All these results indicate that inhibition of
Bcl-xL
expression can result in potent antitumor activity and radiosensitization in human prostatic carcinoma.</description><identifier>ISSN: 0344-5704</identifier><identifier>EISSN: 1432-0843</identifier><identifier>DOI: 10.1007/s00280-007-0548-y</identifier><identifier>PMID: 17653717</identifier><identifier>CODEN: CCPHDZ</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Antineoplastic agents ; Apoptosis - drug effects ; bcl-X Protein - antagonists & inhibitors ; bcl-X Protein - biosynthesis ; bcl-X Protein - genetics ; Biological and medical sciences ; Blotting, Western ; Cancer Research ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Down-Regulation - drug effects ; Flow Cytometry ; Green Fluorescent Proteins - genetics ; Humans ; In Situ Nick-End Labeling ; Luciferases - genetics ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Neoplasm Transplantation ; Nephrology. Urinary tract diseases ; Oncology ; Original Article ; Pharmacology. Drug treatments ; Pharmacology/Toxicology ; Plasmids - genetics ; Promoter Regions, Genetic - genetics ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Radiation-Sensitizing Agents - pharmacology ; Reverse Transcriptase Polymerase Chain Reaction ; RNA Interference - physiology ; Tetrazolium Salts ; Thiazoles ; Transfection ; Transplantation, Heterologous ; Tumor Stem Cell Assay ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>Cancer chemotherapy and pharmacology, 2008-05, Vol.61 (6), p.943-952</ispartof><rights>Springer-Verlag 2007</rights><rights>2008 INIST-CNRS</rights><rights>Springer-Verlag 2008</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c496t-6336cabddc2014f775dd7e665be47ad61655465bec3cfaca691f57f42875c5d73</citedby><cites>FETCH-LOGICAL-c496t-6336cabddc2014f775dd7e665be47ad61655465bec3cfaca691f57f42875c5d73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20200947$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17653717$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Lin, Fang</creatorcontrib><creatorcontrib>Wang, Xi</creatorcontrib><creatorcontrib>Gao, Ping</creatorcontrib><creatorcontrib>Dong, Ke</creatorcontrib><creatorcontrib>Wei, San-Hua</creatorcontrib><creatorcontrib>Cheng, Shi-Yin</creatorcontrib><creatorcontrib>Zhang, Hui-Zhong</creatorcontrib><title>Suppression of Bcl-xL expression by a novel tumor-specific RNA interference system inhibits proliferation and enhances radiosensitivity in prostatic carcinoma cells</title><title>Cancer chemotherapy and pharmacology</title><addtitle>Cancer Chemother Pharmacol</addtitle><addtitle>Cancer Chemother Pharmacol</addtitle><description>Bcl-xL
, a novel member of anti-apoptotic
Bcl-2
family that play important roles in regulating cell survival and apoptosis, is frequently overexpressed in various kinds of human cancers, including prostatic carcinoma. To explore its possibility as a therapeutic target for prostatic carcinoma, we developed a novel tumor-specific RNA interference system by using survivin promoter and employed it to suppress exogenous reporters (
LUC
and
EGFP
) and endogenous gene
Bcl-xL
expression and analyzed its phenotypes. We found that expression of exogenous reporters (
LUC
and
EGFP
) was specifically inhibited in tumor cells but not in normal cells. We also observed that the specific inhibition of
Bcl-xL
in human prostatic carcinoma cells (PC3) strongly suppressed in vitro cell proliferation and in vivo tumorigenicity. We observed significant apoptosis induction and radiosensitivity enhancement in PC3 cells by the RNA interference-mediated suppression of
Bcl-xL
expression. All these results indicate that inhibition of
Bcl-xL
expression can result in potent antitumor activity and radiosensitization in human prostatic carcinoma.</description><subject>Antineoplastic agents</subject><subject>Apoptosis - drug effects</subject><subject>bcl-X Protein - antagonists & inhibitors</subject><subject>bcl-X Protein - biosynthesis</subject><subject>bcl-X Protein - genetics</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cancer Research</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Down-Regulation - drug effects</subject><subject>Flow Cytometry</subject><subject>Green Fluorescent Proteins - genetics</subject><subject>Humans</subject><subject>In Situ Nick-End Labeling</subject><subject>Luciferases - genetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Neoplasm Transplantation</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pharmacology. Drug treatments</subject><subject>Pharmacology/Toxicology</subject><subject>Plasmids - genetics</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Radiation-Sensitizing Agents - pharmacology</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>RNA Interference - physiology</subject><subject>Tetrazolium Salts</subject><subject>Thiazoles</subject><subject>Transfection</subject><subject>Transplantation, Heterologous</subject><subject>Tumor Stem Cell Assay</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Urinary tract diseases</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pharmacology. Drug treatments</topic><topic>Pharmacology/Toxicology</topic><topic>Plasmids - genetics</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Radiation-Sensitizing Agents - pharmacology</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>RNA Interference - physiology</topic><topic>Tetrazolium Salts</topic><topic>Thiazoles</topic><topic>Transfection</topic><topic>Transplantation, Heterologous</topic><topic>Tumor Stem Cell Assay</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Rui</creatorcontrib><creatorcontrib>Lin, Fang</creatorcontrib><creatorcontrib>Wang, Xi</creatorcontrib><creatorcontrib>Gao, Ping</creatorcontrib><creatorcontrib>Dong, Ke</creatorcontrib><creatorcontrib>Wei, San-Hua</creatorcontrib><creatorcontrib>Cheng, Shi-Yin</creatorcontrib><creatorcontrib>Zhang, Hui-Zhong</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>ProQuest Central (Corporate)</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Nucleic Acids Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cancer chemotherapy and pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Rui</au><au>Lin, Fang</au><au>Wang, Xi</au><au>Gao, Ping</au><au>Dong, Ke</au><au>Wei, San-Hua</au><au>Cheng, Shi-Yin</au><au>Zhang, Hui-Zhong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of Bcl-xL expression by a novel tumor-specific RNA interference system inhibits proliferation and enhances radiosensitivity in prostatic carcinoma cells</atitle><jtitle>Cancer chemotherapy and pharmacology</jtitle><stitle>Cancer Chemother Pharmacol</stitle><addtitle>Cancer Chemother Pharmacol</addtitle><date>2008-05-01</date><risdate>2008</risdate><volume>61</volume><issue>6</issue><spage>943</spage><epage>952</epage><pages>943-952</pages><issn>0344-5704</issn><eissn>1432-0843</eissn><coden>CCPHDZ</coden><abstract>Bcl-xL
, a novel member of anti-apoptotic
Bcl-2
family that play important roles in regulating cell survival and apoptosis, is frequently overexpressed in various kinds of human cancers, including prostatic carcinoma. To explore its possibility as a therapeutic target for prostatic carcinoma, we developed a novel tumor-specific RNA interference system by using survivin promoter and employed it to suppress exogenous reporters (
LUC
and
EGFP
) and endogenous gene
Bcl-xL
expression and analyzed its phenotypes. We found that expression of exogenous reporters (
LUC
and
EGFP
) was specifically inhibited in tumor cells but not in normal cells. We also observed that the specific inhibition of
Bcl-xL
in human prostatic carcinoma cells (PC3) strongly suppressed in vitro cell proliferation and in vivo tumorigenicity. We observed significant apoptosis induction and radiosensitivity enhancement in PC3 cells by the RNA interference-mediated suppression of
Bcl-xL
expression. All these results indicate that inhibition of
Bcl-xL
expression can result in potent antitumor activity and radiosensitization in human prostatic carcinoma.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>17653717</pmid><doi>10.1007/s00280-007-0548-y</doi><tpages>10</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0344-5704 |
| ispartof | Cancer chemotherapy and pharmacology, 2008-05, Vol.61 (6), p.943-952 |
| issn | 0344-5704 1432-0843 |
| language | eng |
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| source | Springer Nature |
| subjects | Antineoplastic agents Apoptosis - drug effects bcl-X Protein - antagonists & inhibitors bcl-X Protein - biosynthesis bcl-X Protein - genetics Biological and medical sciences Blotting, Western Cancer Research Cell Line, Tumor Cell Proliferation - drug effects Down-Regulation - drug effects Flow Cytometry Green Fluorescent Proteins - genetics Humans In Situ Nick-End Labeling Luciferases - genetics Male Medical sciences Medicine Medicine & Public Health Neoplasm Transplantation Nephrology. Urinary tract diseases Oncology Original Article Pharmacology. Drug treatments Pharmacology/Toxicology Plasmids - genetics Promoter Regions, Genetic - genetics Prostatic Neoplasms - drug therapy Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Radiation-Sensitizing Agents - pharmacology Reverse Transcriptase Polymerase Chain Reaction RNA Interference - physiology Tetrazolium Salts Thiazoles Transfection Transplantation, Heterologous Tumor Stem Cell Assay Tumors of the urinary system Urinary tract. Prostate gland |
| title | Suppression of Bcl-xL expression by a novel tumor-specific RNA interference system inhibits proliferation and enhances radiosensitivity in prostatic carcinoma cells |
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