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p21 modulates threshold of apoptosis induced by DNA-damage and growth factor withdrawal in prostate cancer cells
Current therapy for advanced prostate cancer is largely based on androgen deprivation and is mostly palliative because all patients eventually relapse with androgen-independent disease. Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a str...
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| Published in: | Carcinogenesis (New York) 2002-08, Vol.23 (8), p.1289-1296 |
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| container_end_page | 1296 |
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| container_title | Carcinogenesis (New York) |
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| creator | Martinez, Luis A. Yang, Jun Vazquez, Elba S. del Carmen Rodriguez-Vargas, María Olive, Matilde Hsieh, Jer-Tsong Logothetis, Christopher J. Navone, Nora M. |
| description | Current therapy for advanced prostate cancer is largely based on androgen deprivation and is mostly palliative because all patients eventually relapse with androgen-independent disease. Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a strong inducer of p53 expression and p21CIP1/WAF1 (p21) transactivation. Previous reports suggest that p21 may have a role in the modulation to chemotherapy-induced apoptosis, prostate cancer progression and androgen regulation. In order to investigate if p21 has a pro-survival role in the response of prostate cancer cells to cellular stress, we exposed two androgen-regulated human prostate cancer cell lines (MDA PCa 2b and LNCaP) to Dx and growth factor withdrawal. We then studied expression of p53 and p21, cell-cycle kinetics and apoptosis. We have found that p53 protein accumulated in a dose- and time-dependent manner after Dx treatment, while p21 expression increased over time with low but decreased with high Dx doses. Apoptosis occurred in parallel with p21 down-modulation. Dx treatment of p53 knockout cells demonstrated that p21 induction was strictly p53 dependent. Reduction of p21 levels in prostate cancer cells with an antisense p21 adenovirus resulted in sensitization to Dx and accelerated onset of apoptosis in response to growth factor withdrawal. The evidence presented here also suggests that caspase activation mediates the apoptosis in this system and supports that p21 may modulate the threshold of apoptosis in prostate cancer. These observations may thus provide implications onto the integration of chemotherapy and androgen ablation. |
| doi_str_mv | 10.1093/carcin/23.8.1289 |
| format | article |
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Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a strong inducer of p53 expression and p21CIP1/WAF1 (p21) transactivation. Previous reports suggest that p21 may have a role in the modulation to chemotherapy-induced apoptosis, prostate cancer progression and androgen regulation. In order to investigate if p21 has a pro-survival role in the response of prostate cancer cells to cellular stress, we exposed two androgen-regulated human prostate cancer cell lines (MDA PCa 2b and LNCaP) to Dx and growth factor withdrawal. We then studied expression of p53 and p21, cell-cycle kinetics and apoptosis. We have found that p53 protein accumulated in a dose- and time-dependent manner after Dx treatment, while p21 expression increased over time with low but decreased with high Dx doses. Apoptosis occurred in parallel with p21 down-modulation. Dx treatment of p53 knockout cells demonstrated that p21 induction was strictly p53 dependent. Reduction of p21 levels in prostate cancer cells with an antisense p21 adenovirus resulted in sensitization to Dx and accelerated onset of apoptosis in response to growth factor withdrawal. The evidence presented here also suggests that caspase activation mediates the apoptosis in this system and supports that p21 may modulate the threshold of apoptosis in prostate cancer. These observations may thus provide implications onto the integration of chemotherapy and androgen ablation.</description><identifier>ISSN: 0143-3334</identifier><identifier>EISSN: 1460-2180</identifier><identifier>DOI: 10.1093/carcin/23.8.1289</identifier><identifier>PMID: 12151346</identifier><identifier>CODEN: CRNGDP</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Antibiotics, Antineoplastic - pharmacology ; Antineoplastic agents ; Apoptosis - physiology ; Biological and medical sciences ; CDK ; Cell Cycle ; Cell Survival ; Chemotherapy ; cyclin-dependent kinase ; Cyclin-Dependent Kinase Inhibitor p21 ; Cyclins - metabolism ; Cyclins - physiology ; Cysteine Proteinase Inhibitors - pharmacology ; DNA Damage ; doxorubicin ; Doxorubicin - pharmacology ; Growth Substances - metabolism ; HPV ; human papillomavirus ; Humans ; Male ; Medical sciences ; MOI ; multiplicities of infection ; Neoplasms, Hormone-Dependent - metabolism ; Neoplasms, Hormone-Dependent - pathology ; Pharmacology. Drug treatments ; Poly(ADP-ribose) Polymerases - metabolism ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Proto-Oncogene Proteins c-bcl-2 - physiology ; terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling ; Tumor Cells, Cultured ; Tumor Suppressor Protein p53 - metabolism ; TUNEL</subject><ispartof>Carcinogenesis (New York), 2002-08, Vol.23 (8), p.1289-1296</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Aug 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c529t-d61c8908262eee091bf96d4d96ad974021f2a8e303b1d70380dcf1868e3cbed93</citedby><cites>FETCH-LOGICAL-c529t-d61c8908262eee091bf96d4d96ad974021f2a8e303b1d70380dcf1868e3cbed93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13822960$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12151346$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martinez, Luis A.</creatorcontrib><creatorcontrib>Yang, Jun</creatorcontrib><creatorcontrib>Vazquez, Elba S.</creatorcontrib><creatorcontrib>del Carmen Rodriguez-Vargas, María</creatorcontrib><creatorcontrib>Olive, Matilde</creatorcontrib><creatorcontrib>Hsieh, Jer-Tsong</creatorcontrib><creatorcontrib>Logothetis, Christopher J.</creatorcontrib><creatorcontrib>Navone, Nora M.</creatorcontrib><title>p21 modulates threshold of apoptosis induced by DNA-damage and growth factor withdrawal in prostate cancer cells</title><title>Carcinogenesis (New York)</title><addtitle>Carcinogenesis</addtitle><description>Current therapy for advanced prostate cancer is largely based on androgen deprivation and is mostly palliative because all patients eventually relapse with androgen-independent disease. Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a strong inducer of p53 expression and p21CIP1/WAF1 (p21) transactivation. Previous reports suggest that p21 may have a role in the modulation to chemotherapy-induced apoptosis, prostate cancer progression and androgen regulation. In order to investigate if p21 has a pro-survival role in the response of prostate cancer cells to cellular stress, we exposed two androgen-regulated human prostate cancer cell lines (MDA PCa 2b and LNCaP) to Dx and growth factor withdrawal. We then studied expression of p53 and p21, cell-cycle kinetics and apoptosis. We have found that p53 protein accumulated in a dose- and time-dependent manner after Dx treatment, while p21 expression increased over time with low but decreased with high Dx doses. Apoptosis occurred in parallel with p21 down-modulation. Dx treatment of p53 knockout cells demonstrated that p21 induction was strictly p53 dependent. Reduction of p21 levels in prostate cancer cells with an antisense p21 adenovirus resulted in sensitization to Dx and accelerated onset of apoptosis in response to growth factor withdrawal. The evidence presented here also suggests that caspase activation mediates the apoptosis in this system and supports that p21 may modulate the threshold of apoptosis in prostate cancer. These observations may thus provide implications onto the integration of chemotherapy and androgen ablation.</description><subject>Antibiotics, Antineoplastic - pharmacology</subject><subject>Antineoplastic agents</subject><subject>Apoptosis - physiology</subject><subject>Biological and medical sciences</subject><subject>CDK</subject><subject>Cell Cycle</subject><subject>Cell Survival</subject><subject>Chemotherapy</subject><subject>cyclin-dependent kinase</subject><subject>Cyclin-Dependent Kinase Inhibitor p21</subject><subject>Cyclins - metabolism</subject><subject>Cyclins - physiology</subject><subject>Cysteine Proteinase Inhibitors - pharmacology</subject><subject>DNA Damage</subject><subject>doxorubicin</subject><subject>Doxorubicin - pharmacology</subject><subject>Growth Substances - metabolism</subject><subject>HPV</subject><subject>human papillomavirus</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>MOI</subject><subject>multiplicities of infection</subject><subject>Neoplasms, Hormone-Dependent - metabolism</subject><subject>Neoplasms, Hormone-Dependent - pathology</subject><subject>Pharmacology. Drug treatments</subject><subject>Poly(ADP-ribose) Polymerases - metabolism</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - physiology</subject><subject>terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling</subject><subject>Tumor Cells, Cultured</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><subject>TUNEL</subject><issn>0143-3334</issn><issn>1460-2180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><recordid>eNpdkc1v1DAQxS0EokvhzglZSHDL1mMnjn0s5aOgApciEBdrYjvdlGwcbEdL_3u82hWVOI3k-b2n53mEPAe2BqbFmcVoh-mMi7VaA1f6AVlBLVnFQbGHZMWgFpUQoj4hT1K6ZQykaPRjcgIcGhC1XJF55kC3wS0jZp9o3kSfNmF0NPQU5zDnkIZEh8kt1jva3dG3X84rh1u88RQnR29i2OUN7dHmEOluyBsXcYdjkdA5hpSLLbU4WR-p9eOYnpJHPY7JPzvOU_Lt_bvri8vq6uuHjxfnV5VtuM6Vk2CVZopL7r1nGrpeS1c7LdHptmYceo7KCyY6cC0Tijnbg5LlyXbeaXFKXh98S4rfi0_ZbIe0T4CTD0syUETFCAr48j_wNixxKtkMB821aHVbIHaAbPlTir43cxy2GO8MMLOvwhyqMFwYZfZVFMmLo-_Sbb27FxxvX4BXRwCTxbGP5UpDuueE4lxLVrjqwA0p-z__9hh_GdmKtjGXP34aaL5_ltdvtPkk_gKBo6Iz</recordid><startdate>20020801</startdate><enddate>20020801</enddate><creator>Martinez, Luis A.</creator><creator>Yang, Jun</creator><creator>Vazquez, Elba S.</creator><creator>del Carmen Rodriguez-Vargas, María</creator><creator>Olive, Matilde</creator><creator>Hsieh, Jer-Tsong</creator><creator>Logothetis, Christopher J.</creator><creator>Navone, Nora M.</creator><general>Oxford University Press</general><general>Oxford Publishing Limited (England)</general><scope>BSCLL</scope><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>7T5</scope><scope>7TM</scope><scope>7TO</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20020801</creationdate><title>p21 modulates threshold of apoptosis induced by DNA-damage and growth factor withdrawal in prostate cancer cells</title><author>Martinez, Luis A. ; Yang, Jun ; Vazquez, Elba S. ; del Carmen Rodriguez-Vargas, María ; Olive, Matilde ; Hsieh, Jer-Tsong ; Logothetis, Christopher J. ; Navone, Nora M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c529t-d61c8908262eee091bf96d4d96ad974021f2a8e303b1d70380dcf1868e3cbed93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Antibiotics, Antineoplastic - pharmacology</topic><topic>Antineoplastic agents</topic><topic>Apoptosis - physiology</topic><topic>Biological and medical sciences</topic><topic>CDK</topic><topic>Cell Cycle</topic><topic>Cell Survival</topic><topic>Chemotherapy</topic><topic>cyclin-dependent kinase</topic><topic>Cyclin-Dependent Kinase Inhibitor p21</topic><topic>Cyclins - metabolism</topic><topic>Cyclins - physiology</topic><topic>Cysteine Proteinase Inhibitors - pharmacology</topic><topic>DNA Damage</topic><topic>doxorubicin</topic><topic>Doxorubicin - pharmacology</topic><topic>Growth Substances - metabolism</topic><topic>HPV</topic><topic>human papillomavirus</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>MOI</topic><topic>multiplicities of infection</topic><topic>Neoplasms, Hormone-Dependent - metabolism</topic><topic>Neoplasms, Hormone-Dependent - pathology</topic><topic>Pharmacology. Drug treatments</topic><topic>Poly(ADP-ribose) Polymerases - metabolism</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - physiology</topic><topic>terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling</topic><topic>Tumor Cells, Cultured</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><topic>TUNEL</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martinez, Luis A.</creatorcontrib><creatorcontrib>Yang, Jun</creatorcontrib><creatorcontrib>Vazquez, Elba S.</creatorcontrib><creatorcontrib>del Carmen Rodriguez-Vargas, María</creatorcontrib><creatorcontrib>Olive, Matilde</creatorcontrib><creatorcontrib>Hsieh, Jer-Tsong</creatorcontrib><creatorcontrib>Logothetis, Christopher J.</creatorcontrib><creatorcontrib>Navone, Nora M.</creatorcontrib><collection>Istex</collection><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>Immunology Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Carcinogenesis (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martinez, Luis A.</au><au>Yang, Jun</au><au>Vazquez, Elba S.</au><au>del Carmen Rodriguez-Vargas, María</au><au>Olive, Matilde</au><au>Hsieh, Jer-Tsong</au><au>Logothetis, Christopher J.</au><au>Navone, Nora M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p21 modulates threshold of apoptosis induced by DNA-damage and growth factor withdrawal in prostate cancer cells</atitle><jtitle>Carcinogenesis (New York)</jtitle><addtitle>Carcinogenesis</addtitle><date>2002-08-01</date><risdate>2002</risdate><volume>23</volume><issue>8</issue><spage>1289</spage><epage>1296</epage><pages>1289-1296</pages><issn>0143-3334</issn><eissn>1460-2180</eissn><coden>CRNGDP</coden><notes>PII:1460-2180</notes><notes>local:0231289</notes><notes>istex:7279FA426E1A995C47C99F79CE21D2A22D302697</notes><notes>ark:/67375/HXZ-15WM6TB9-J</notes><notes>ObjectType-Article-2</notes><notes>SourceType-Scholarly Journals-1</notes><notes>ObjectType-Feature-1</notes><notes>content type line 23</notes><abstract>Current therapy for advanced prostate cancer is largely based on androgen deprivation and is mostly palliative because all patients eventually relapse with androgen-independent disease. Doxorubicin (Dx), an anthracycline used commonly as a chemotherapeutic agent in relapsed prostate cancer, is a strong inducer of p53 expression and p21CIP1/WAF1 (p21) transactivation. Previous reports suggest that p21 may have a role in the modulation to chemotherapy-induced apoptosis, prostate cancer progression and androgen regulation. In order to investigate if p21 has a pro-survival role in the response of prostate cancer cells to cellular stress, we exposed two androgen-regulated human prostate cancer cell lines (MDA PCa 2b and LNCaP) to Dx and growth factor withdrawal. We then studied expression of p53 and p21, cell-cycle kinetics and apoptosis. We have found that p53 protein accumulated in a dose- and time-dependent manner after Dx treatment, while p21 expression increased over time with low but decreased with high Dx doses. Apoptosis occurred in parallel with p21 down-modulation. Dx treatment of p53 knockout cells demonstrated that p21 induction was strictly p53 dependent. Reduction of p21 levels in prostate cancer cells with an antisense p21 adenovirus resulted in sensitization to Dx and accelerated onset of apoptosis in response to growth factor withdrawal. The evidence presented here also suggests that caspase activation mediates the apoptosis in this system and supports that p21 may modulate the threshold of apoptosis in prostate cancer. These observations may thus provide implications onto the integration of chemotherapy and androgen ablation.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>12151346</pmid><doi>10.1093/carcin/23.8.1289</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antibiotics, Antineoplastic - pharmacology Antineoplastic agents Apoptosis - physiology Biological and medical sciences CDK Cell Cycle Cell Survival Chemotherapy cyclin-dependent kinase Cyclin-Dependent Kinase Inhibitor p21 Cyclins - metabolism Cyclins - physiology Cysteine Proteinase Inhibitors - pharmacology DNA Damage doxorubicin Doxorubicin - pharmacology Growth Substances - metabolism HPV human papillomavirus Humans Male Medical sciences MOI multiplicities of infection Neoplasms, Hormone-Dependent - metabolism Neoplasms, Hormone-Dependent - pathology Pharmacology. Drug treatments Poly(ADP-ribose) Polymerases - metabolism Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Proto-Oncogene Proteins c-bcl-2 - physiology terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling Tumor Cells, Cultured Tumor Suppressor Protein p53 - metabolism TUNEL |
| title | p21 modulates threshold of apoptosis induced by DNA-damage and growth factor withdrawal in prostate cancer cells |
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