p53 Regulates the Expression of the Tumor Suppressor Gene Maspin
Maspin has been shown to inhibit tumor cell invasion and metastasis in breast tumor cells. Maspin expression was detected in normal breast and prostate epithelial cells, whereas tumor cells exhibited reduced or no expression. However, the regulatory mechanism of maspin expression remains unknown. We...
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| Veröffentlicht in: | The Journal of biological chemistry 2000-03, Vol.275 (9), p.6051-6054 |
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| container_title | The Journal of biological chemistry |
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| creator | Zou, Zhiqiang Gao, Chunling Nagaich, Akhilesh K. Connell, Theresa Saito, Shin'ichi Moul, Judd W. Seth, Prem Appella, Ettore Srivastava, Shiv |
| description | Maspin has been shown to inhibit tumor cell invasion and metastasis in breast tumor cells. Maspin expression was detected in normal breast and prostate epithelial cells, whereas tumor cells exhibited reduced or no expression. However, the regulatory mechanism of maspin expression remains unknown. We report here a rapid and robust induction of maspin expression in prostate cancer cells (LNCaP, DU145, and PC3) and breast tumor cells (MCF7) following wild type p53 expression from an adenovirus p53 expression vector (AdWTp53). p53 activates the maspin promoter by binding directly to the p53 consensus-binding site present in the maspin promoter. DNA-damaging agents and cytotoxic drugs induced endogenous maspin expression in cells containing the wild type p53. Maspin expression was refractory to the DNA-damaging agents in cells containing mutant p53. These results, combined with recent studies of the tumor metastasis suppressor geneKAI1 and plasminogen activator inhibitor 1 (PAI1), define a new category of molecular targets of p53 that have the potential to negatively regulate tumor invasion and/or metastasis. |
| doi_str_mv | 10.1074/jbc.275.9.6051 |
| format | Article |
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Maspin expression was detected in normal breast and prostate epithelial cells, whereas tumor cells exhibited reduced or no expression. However, the regulatory mechanism of maspin expression remains unknown. We report here a rapid and robust induction of maspin expression in prostate cancer cells (LNCaP, DU145, and PC3) and breast tumor cells (MCF7) following wild type p53 expression from an adenovirus p53 expression vector (AdWTp53). p53 activates the maspin promoter by binding directly to the p53 consensus-binding site present in the maspin promoter. DNA-damaging agents and cytotoxic drugs induced endogenous maspin expression in cells containing the wild type p53. Maspin expression was refractory to the DNA-damaging agents in cells containing mutant p53. These results, combined with recent studies of the tumor metastasis suppressor geneKAI1 and plasminogen activator inhibitor 1 (PAI1), define a new category of molecular targets of p53 that have the potential to negatively regulate tumor invasion and/or metastasis.</description><identifier>ISSN: 0021-9258</identifier><identifier>EISSN: 1083-351X</identifier><identifier>DOI: 10.1074/jbc.275.9.6051</identifier><identifier>PMID: 10692390</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>adeno-associated virus ; Adenoviridae - genetics ; Antineoplastic Agents - pharmacology ; Breast Neoplasms - metabolism ; DNA Damage - drug effects ; DNA Damage - radiation effects ; DNA-Binding Proteins - metabolism ; Etoposide - pharmacology ; Gene Expression Regulation ; Gene Expression Regulation, Neoplastic - drug effects ; Genes, Tumor Suppressor - drug effects ; Humans ; Male ; maspin ; Neoplasm Metastasis ; Promoter Regions, Genetic ; Prostatic Neoplasms - metabolism ; Proteins - pharmacology ; RNA, Messenger - metabolism ; Serpins - pharmacology ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53 - genetics ; Tumor Suppressor Protein p53 - metabolism ; Ultraviolet Rays</subject><ispartof>The Journal of biological chemistry, 2000-03, Vol.275 (9), p.6051-6054</ispartof><rights>2000 © 2000 ASBMB. 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Maspin expression was detected in normal breast and prostate epithelial cells, whereas tumor cells exhibited reduced or no expression. However, the regulatory mechanism of maspin expression remains unknown. We report here a rapid and robust induction of maspin expression in prostate cancer cells (LNCaP, DU145, and PC3) and breast tumor cells (MCF7) following wild type p53 expression from an adenovirus p53 expression vector (AdWTp53). p53 activates the maspin promoter by binding directly to the p53 consensus-binding site present in the maspin promoter. DNA-damaging agents and cytotoxic drugs induced endogenous maspin expression in cells containing the wild type p53. Maspin expression was refractory to the DNA-damaging agents in cells containing mutant p53. These results, combined with recent studies of the tumor metastasis suppressor geneKAI1 and plasminogen activator inhibitor 1 (PAI1), define a new category of molecular targets of p53 that have the potential to negatively regulate tumor invasion and/or metastasis.</description><subject>adeno-associated virus</subject><subject>Adenoviridae - genetics</subject><subject>Antineoplastic Agents - pharmacology</subject><subject>Breast Neoplasms - metabolism</subject><subject>DNA Damage - drug effects</subject><subject>DNA Damage - radiation effects</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Etoposide - pharmacology</subject><subject>Gene Expression Regulation</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Genes, Tumor Suppressor - drug effects</subject><subject>Humans</subject><subject>Male</subject><subject>maspin</subject><subject>Neoplasm Metastasis</subject><subject>Promoter Regions, Genetic</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Proteins - pharmacology</subject><subject>RNA, Messenger - metabolism</subject><subject>Serpins - pharmacology</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Protein p53 - genetics</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>Ultraviolet Rays</subject><issn>0021-9258</issn><issn>1083-351X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kDtPwzAURi0EoqWwMqKIgS3BjuMk3kBVKUhFSFAkNstxbhpXzQM74fHvcZsOMODF1r3n-2QdhM4JDghOout1poIwYQEPYszIARoTnFKfMvJ2iMYYh8TnIUtH6MTaNXYn4uQYjQiOeUg5HqObllHvGVb9RnZgva4Eb_bVGrBWN7XXFLvJsq8a47307W7hnnOowXuUttX1KToq5MbC2f6eoNe72XJ67y-e5g_T24WvIpp2PmRREsWhDIHnUmVAMkoJASJJQmmsIpwxxqVkBVVJnqoo4TkDDinlOcQqzekEXQ29rWnee7CdqLRVsNnIGpreCpIwTKMwdmAwgMo01hooRGt0Jc23IFhsnQnnTDhngoutMxe42Df3WQX5L3yQ5IDLASj1qvzUBkSmG1VC9bclHSBwEj40GGGVhlpB7gKqE3mj__vADztJhY8</recordid><startdate>20000303</startdate><enddate>20000303</enddate><creator>Zou, Zhiqiang</creator><creator>Gao, Chunling</creator><creator>Nagaich, Akhilesh K.</creator><creator>Connell, Theresa</creator><creator>Saito, Shin'ichi</creator><creator>Moul, Judd W.</creator><creator>Seth, Prem</creator><creator>Appella, Ettore</creator><creator>Srivastava, Shiv</creator><general>Elsevier Inc</general><general>American Society for Biochemistry and Molecular Biology</general><scope>6I.</scope><scope>AAFTH</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>7TM</scope><scope>7TO</scope><scope>H94</scope></search><sort><creationdate>20000303</creationdate><title>p53 Regulates the Expression of the Tumor Suppressor Gene Maspin</title><author>Zou, Zhiqiang ; 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Maspin expression was detected in normal breast and prostate epithelial cells, whereas tumor cells exhibited reduced or no expression. However, the regulatory mechanism of maspin expression remains unknown. We report here a rapid and robust induction of maspin expression in prostate cancer cells (LNCaP, DU145, and PC3) and breast tumor cells (MCF7) following wild type p53 expression from an adenovirus p53 expression vector (AdWTp53). p53 activates the maspin promoter by binding directly to the p53 consensus-binding site present in the maspin promoter. DNA-damaging agents and cytotoxic drugs induced endogenous maspin expression in cells containing the wild type p53. Maspin expression was refractory to the DNA-damaging agents in cells containing mutant p53. 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| subjects | adeno-associated virus Adenoviridae - genetics Antineoplastic Agents - pharmacology Breast Neoplasms - metabolism DNA Damage - drug effects DNA Damage - radiation effects DNA-Binding Proteins - metabolism Etoposide - pharmacology Gene Expression Regulation Gene Expression Regulation, Neoplastic - drug effects Genes, Tumor Suppressor - drug effects Humans Male maspin Neoplasm Metastasis Promoter Regions, Genetic Prostatic Neoplasms - metabolism Proteins - pharmacology RNA, Messenger - metabolism Serpins - pharmacology Tumor Cells, Cultured Tumor Suppressor Protein p53 - genetics Tumor Suppressor Protein p53 - metabolism Ultraviolet Rays |
| title | p53 Regulates the Expression of the Tumor Suppressor Gene Maspin |
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