Potential Mechanism for the Effects of Dexamethasone on Growth of Androgen-Independent Prostate Cancer
Background: Dexamethasone, a synthetic glucocorticoid, has clinical benefit in patients with hormone-refractory prostate cancer (HRPC), but the mechanisms responsible for its effects are unknown. The nuclear factor-κB (NF-κB)-dependent cytokine interleukin (IL) 6 (IL-6) is thought to stimulate growt...
Gespeichert in:
| Veröffentlicht in: | JNCI : Journal of the National Cancer Institute 2001-11, Vol.93 (22), p.1739-1746 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1746 |
|---|---|
| container_issue | 22 |
| container_start_page | 1739 |
| container_title | JNCI : Journal of the National Cancer Institute |
| container_volume | 93 |
| creator | Nishimura, Kazuo Nonomura, Norio Satoh, Eiichi Harada, Yasunori Nakayama, Masashi Tokizane, Takashi Fukui, Tatsunari Ono, Yutaka Inoue, Hitoshi Shin, Masaru Tsujimoto, Yuichi Takayama, Hitoshi Aozasa, Katsuyuki Okuyama, Akihiko |
| description | Background: Dexamethasone, a synthetic glucocorticoid, has clinical benefit in patients with hormone-refractory prostate cancer (HRPC), but the mechanisms responsible for its effects are unknown. The nuclear factor-κB (NF-κB)-dependent cytokine interleukin (IL) 6 (IL-6) is thought to stimulate growth of HRPC. Because dexamethasone interferes with NF-κB activation, we determined whether dexamethasone inhibits prostate cancer growth by working through the glucocorticoid receptor (GR) to interfere with NF-κB–IL-6 pathway. Methods: Three human prostate cancer cell lines (DU145, PC-3, and LNCaP) were assessed for GR expression and responsiveness to dexamethasone. Levels of GR, NF-κβ, and the cytoplasmic NF-κβ inhibitor IκBα were determined by western blotting and of IL-6 by enzyme immunoassay. The subcellular localization of NF-κβ was analyzed by immunofluorescence. The effects of dexamethasone (thrice weekly injections of 1 μg/mouse) on DU145 xenografts in nude and severe combined immunodeficient (SCID) mice were evaluated. GR expression in human prostate cancers was assessed by immunohistochemistry. All statistical tests were two-sided. Results: Dexamethasone dose dependently decreased GR levels and inhibited the growth of DU145 and PC-3 but not LNCaP cells (DU145 cells, P |
| doi_str_mv | 10.1093/jnci/93.22.1739 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_72295146</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>72295146</sourcerecordid><originalsourceid>FETCH-LOGICAL-c427t-330f373fcc64214629f8694845348d95c64743a492658e5c8e5bfe1262a8fe5e3</originalsourceid><addsrcrecordid>eNpdkE1vEzEQhi0EomnhzA1ZSHDbxJ_r9bFKS1OpiB5AoF4s1xmTDbt2ajui_fd4lYhKjOQZyfPMa8-L0DtK5pRovtgG1y80nzM2p4rrF2hGRUsaRol8iWaEMNV0nRIn6DTnLamhmXiNTihVFedyhvxtLBBKbwf8BdzGhj6P2MeEywbwpffgSsbR4wt4tCOUjc0xAI4BX6X4p2ym1nlYp_gLQnMd1rCDmkLBtynmYgvgpQ0O0hv0ytshw9tjPUPfP19-W66am69X18vzm8YJpkrDOfFcce9cK1jdhGnftVp0QnLRrbWs10pwKzRrZQfS1XPvgbKW2c6DBH6GPh10dyk-7CEXM_bZwTDYAHGfjWJMyypcwQ__gdu4T6H-zTBGtFIt6yq0OECubpMTeLNL_WjTk6HETP6byX9TK2Nm8r9OvD_K7u9HWD_zR8Mr8PEI2Ozs4FO1p8_PnKCcKT493Ry4Phd4_Ne36bdpFVfSrH7embb9sRLqojN3_C8wiJxA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>220977628</pqid></control><display><type>article</type><title>Potential Mechanism for the Effects of Dexamethasone on Growth of Androgen-Independent Prostate Cancer</title><source>Oxford University Press Journals All Titles (1996-Current)</source><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Nishimura, Kazuo ; Nonomura, Norio ; Satoh, Eiichi ; Harada, Yasunori ; Nakayama, Masashi ; Tokizane, Takashi ; Fukui, Tatsunari ; Ono, Yutaka ; Inoue, Hitoshi ; Shin, Masaru ; Tsujimoto, Yuichi ; Takayama, Hitoshi ; Aozasa, Katsuyuki ; Okuyama, Akihiko</creator><creatorcontrib>Nishimura, Kazuo ; Nonomura, Norio ; Satoh, Eiichi ; Harada, Yasunori ; Nakayama, Masashi ; Tokizane, Takashi ; Fukui, Tatsunari ; Ono, Yutaka ; Inoue, Hitoshi ; Shin, Masaru ; Tsujimoto, Yuichi ; Takayama, Hitoshi ; Aozasa, Katsuyuki ; Okuyama, Akihiko</creatorcontrib><description>Background: Dexamethasone, a synthetic glucocorticoid, has clinical benefit in patients with hormone-refractory prostate cancer (HRPC), but the mechanisms responsible for its effects are unknown. The nuclear factor-κB (NF-κB)-dependent cytokine interleukin (IL) 6 (IL-6) is thought to stimulate growth of HRPC. Because dexamethasone interferes with NF-κB activation, we determined whether dexamethasone inhibits prostate cancer growth by working through the glucocorticoid receptor (GR) to interfere with NF-κB–IL-6 pathway. Methods: Three human prostate cancer cell lines (DU145, PC-3, and LNCaP) were assessed for GR expression and responsiveness to dexamethasone. Levels of GR, NF-κβ, and the cytoplasmic NF-κβ inhibitor IκBα were determined by western blotting and of IL-6 by enzyme immunoassay. The subcellular localization of NF-κβ was analyzed by immunofluorescence. The effects of dexamethasone (thrice weekly injections of 1 μg/mouse) on DU145 xenografts in nude and severe combined immunodeficient (SCID) mice were evaluated. GR expression in human prostate cancers was assessed by immunohistochemistry. All statistical tests were two-sided. Results: Dexamethasone dose dependently decreased GR levels and inhibited the growth of DU145 and PC-3 but not LNCaP cells (DU145 cells, P<.001; PC-3 cells, P = .009). Dexamethasone increased IκBα protein levels and the cytosolic accumulation of NF-κB in DU145 cells and decreased secreted IL-6 levels to 37 pg/mL (95% confidence interval [CI] = 33 pg/mL to 41 pg/mL), compared with 164 pg/mL (95% CI = 162 pg/mL to 166 pg/mL) secreted by ethanol-treated control cells. Dexamethasone inhibited the growth of DU145 xenografts in nude (P = .006) and SCID (P = .026) mice without affecting GR levels. Eight of 16 human prostate cancers expressed GR at high levels (≥30% GR-positive cells). Conclusion: Dexamethasone inhibited the growth of GR-positive cancers, possibly through the disruption of the NF-κB–IL-6 pathway.</description><identifier>ISSN: 0027-8874</identifier><identifier>EISSN: 1460-2105</identifier><identifier>DOI: 10.1093/jnci/93.22.1739</identifier><identifier>PMID: 11717335</identifier><identifier>CODEN: JNCIEQ</identifier><language>eng</language><publisher>Cary, NC: Oxford University Press</publisher><subject>Androgens - physiology ; Animals ; Biological and medical sciences ; Blotting, Western ; Cell Division - drug effects ; Dexamethasone - pharmacology ; DNA-Binding Proteins - metabolism ; Humans ; I-kappa B Proteins ; Interleukin-6 - metabolism ; Male ; Medical sciences ; Mice ; Mice, Nude ; Models, Animal ; Neoplasm Transplantation ; Nephrology. Urinary tract diseases ; NF-kappa B - metabolism ; NF-KappaB Inhibitor alpha ; Prostatic Neoplasms - metabolism ; Prostatic Neoplasms - pathology ; Receptors, Glucocorticoid - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Transfection ; Transplantation, Heterologous - pathology ; Tumor Cells, Cultured ; Tumors of the urinary system ; Urinary tract. Prostate gland</subject><ispartof>JNCI : Journal of the National Cancer Institute, 2001-11, Vol.93 (22), p.1739-1746</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright Oxford University Press(England) Nov 21, 2001</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-330f373fcc64214629f8694845348d95c64743a492658e5c8e5bfe1262a8fe5e3</citedby><cites>FETCH-LOGICAL-c427t-330f373fcc64214629f8694845348d95c64743a492658e5c8e5bfe1262a8fe5e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14132738$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11717335$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nishimura, Kazuo</creatorcontrib><creatorcontrib>Nonomura, Norio</creatorcontrib><creatorcontrib>Satoh, Eiichi</creatorcontrib><creatorcontrib>Harada, Yasunori</creatorcontrib><creatorcontrib>Nakayama, Masashi</creatorcontrib><creatorcontrib>Tokizane, Takashi</creatorcontrib><creatorcontrib>Fukui, Tatsunari</creatorcontrib><creatorcontrib>Ono, Yutaka</creatorcontrib><creatorcontrib>Inoue, Hitoshi</creatorcontrib><creatorcontrib>Shin, Masaru</creatorcontrib><creatorcontrib>Tsujimoto, Yuichi</creatorcontrib><creatorcontrib>Takayama, Hitoshi</creatorcontrib><creatorcontrib>Aozasa, Katsuyuki</creatorcontrib><creatorcontrib>Okuyama, Akihiko</creatorcontrib><title>Potential Mechanism for the Effects of Dexamethasone on Growth of Androgen-Independent Prostate Cancer</title><title>JNCI : Journal of the National Cancer Institute</title><addtitle>JNCI J Natl Cancer Inst</addtitle><description>Background: Dexamethasone, a synthetic glucocorticoid, has clinical benefit in patients with hormone-refractory prostate cancer (HRPC), but the mechanisms responsible for its effects are unknown. The nuclear factor-κB (NF-κB)-dependent cytokine interleukin (IL) 6 (IL-6) is thought to stimulate growth of HRPC. Because dexamethasone interferes with NF-κB activation, we determined whether dexamethasone inhibits prostate cancer growth by working through the glucocorticoid receptor (GR) to interfere with NF-κB–IL-6 pathway. Methods: Three human prostate cancer cell lines (DU145, PC-3, and LNCaP) were assessed for GR expression and responsiveness to dexamethasone. Levels of GR, NF-κβ, and the cytoplasmic NF-κβ inhibitor IκBα were determined by western blotting and of IL-6 by enzyme immunoassay. The subcellular localization of NF-κβ was analyzed by immunofluorescence. The effects of dexamethasone (thrice weekly injections of 1 μg/mouse) on DU145 xenografts in nude and severe combined immunodeficient (SCID) mice were evaluated. GR expression in human prostate cancers was assessed by immunohistochemistry. All statistical tests were two-sided. Results: Dexamethasone dose dependently decreased GR levels and inhibited the growth of DU145 and PC-3 but not LNCaP cells (DU145 cells, P<.001; PC-3 cells, P = .009). Dexamethasone increased IκBα protein levels and the cytosolic accumulation of NF-κB in DU145 cells and decreased secreted IL-6 levels to 37 pg/mL (95% confidence interval [CI] = 33 pg/mL to 41 pg/mL), compared with 164 pg/mL (95% CI = 162 pg/mL to 166 pg/mL) secreted by ethanol-treated control cells. Dexamethasone inhibited the growth of DU145 xenografts in nude (P = .006) and SCID (P = .026) mice without affecting GR levels. Eight of 16 human prostate cancers expressed GR at high levels (≥30% GR-positive cells). Conclusion: Dexamethasone inhibited the growth of GR-positive cancers, possibly through the disruption of the NF-κB–IL-6 pathway.</description><subject>Androgens - physiology</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blotting, Western</subject><subject>Cell Division - drug effects</subject><subject>Dexamethasone - pharmacology</subject><subject>DNA-Binding Proteins - metabolism</subject><subject>Humans</subject><subject>I-kappa B Proteins</subject><subject>Interleukin-6 - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Nude</subject><subject>Models, Animal</subject><subject>Neoplasm Transplantation</subject><subject>Nephrology. Urinary tract diseases</subject><subject>NF-kappa B - metabolism</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>Prostatic Neoplasms - metabolism</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Transfection</subject><subject>Transplantation, Heterologous - pathology</subject><subject>Tumor Cells, Cultured</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. Prostate gland</subject><issn>0027-8874</issn><issn>1460-2105</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1vEzEQhi0EomnhzA1ZSHDbxJ_r9bFKS1OpiB5AoF4s1xmTDbt2ajui_fd4lYhKjOQZyfPMa8-L0DtK5pRovtgG1y80nzM2p4rrF2hGRUsaRol8iWaEMNV0nRIn6DTnLamhmXiNTihVFedyhvxtLBBKbwf8BdzGhj6P2MeEywbwpffgSsbR4wt4tCOUjc0xAI4BX6X4p2ym1nlYp_gLQnMd1rCDmkLBtynmYgvgpQ0O0hv0ytshw9tjPUPfP19-W66am69X18vzm8YJpkrDOfFcce9cK1jdhGnftVp0QnLRrbWs10pwKzRrZQfS1XPvgbKW2c6DBH6GPh10dyk-7CEXM_bZwTDYAHGfjWJMyypcwQ__gdu4T6H-zTBGtFIt6yq0OECubpMTeLNL_WjTk6HETP6byX9TK2Nm8r9OvD_K7u9HWD_zR8Mr8PEI2Ozs4FO1p8_PnKCcKT493Ry4Phd4_Ne36bdpFVfSrH7embb9sRLqojN3_C8wiJxA</recordid><startdate>20011121</startdate><enddate>20011121</enddate><creator>Nishimura, Kazuo</creator><creator>Nonomura, Norio</creator><creator>Satoh, Eiichi</creator><creator>Harada, Yasunori</creator><creator>Nakayama, Masashi</creator><creator>Tokizane, Takashi</creator><creator>Fukui, Tatsunari</creator><creator>Ono, Yutaka</creator><creator>Inoue, Hitoshi</creator><creator>Shin, Masaru</creator><creator>Tsujimoto, Yuichi</creator><creator>Takayama, Hitoshi</creator><creator>Aozasa, Katsuyuki</creator><creator>Okuyama, Akihiko</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>7TO</scope><scope>7U7</scope><scope>7U9</scope><scope>C1K</scope><scope>H94</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20011121</creationdate><title>Potential Mechanism for the Effects of Dexamethasone on Growth of Androgen-Independent Prostate Cancer</title><author>Nishimura, Kazuo ; Nonomura, Norio ; Satoh, Eiichi ; Harada, Yasunori ; Nakayama, Masashi ; Tokizane, Takashi ; Fukui, Tatsunari ; Ono, Yutaka ; Inoue, Hitoshi ; Shin, Masaru ; Tsujimoto, Yuichi ; Takayama, Hitoshi ; Aozasa, Katsuyuki ; Okuyama, Akihiko</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-330f373fcc64214629f8694845348d95c64743a492658e5c8e5bfe1262a8fe5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Androgens - physiology</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blotting, Western</topic><topic>Cell Division - drug effects</topic><topic>Dexamethasone - pharmacology</topic><topic>DNA-Binding Proteins - metabolism</topic><topic>Humans</topic><topic>I-kappa B Proteins</topic><topic>Interleukin-6 - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Nude</topic><topic>Models, Animal</topic><topic>Neoplasm Transplantation</topic><topic>Nephrology. Urinary tract diseases</topic><topic>NF-kappa B - metabolism</topic><topic>NF-KappaB Inhibitor alpha</topic><topic>Prostatic Neoplasms - metabolism</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>Reverse Transcriptase Polymerase Chain Reaction</topic><topic>Transfection</topic><topic>Transplantation, Heterologous - pathology</topic><topic>Tumor Cells, Cultured</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nishimura, Kazuo</creatorcontrib><creatorcontrib>Nonomura, Norio</creatorcontrib><creatorcontrib>Satoh, Eiichi</creatorcontrib><creatorcontrib>Harada, Yasunori</creatorcontrib><creatorcontrib>Nakayama, Masashi</creatorcontrib><creatorcontrib>Tokizane, Takashi</creatorcontrib><creatorcontrib>Fukui, Tatsunari</creatorcontrib><creatorcontrib>Ono, Yutaka</creatorcontrib><creatorcontrib>Inoue, Hitoshi</creatorcontrib><creatorcontrib>Shin, Masaru</creatorcontrib><creatorcontrib>Tsujimoto, Yuichi</creatorcontrib><creatorcontrib>Takayama, Hitoshi</creatorcontrib><creatorcontrib>Aozasa, Katsuyuki</creatorcontrib><creatorcontrib>Okuyama, Akihiko</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>Oncogenes and Growth Factors Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>JNCI : Journal of the National Cancer Institute</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nishimura, Kazuo</au><au>Nonomura, Norio</au><au>Satoh, Eiichi</au><au>Harada, Yasunori</au><au>Nakayama, Masashi</au><au>Tokizane, Takashi</au><au>Fukui, Tatsunari</au><au>Ono, Yutaka</au><au>Inoue, Hitoshi</au><au>Shin, Masaru</au><au>Tsujimoto, Yuichi</au><au>Takayama, Hitoshi</au><au>Aozasa, Katsuyuki</au><au>Okuyama, Akihiko</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Potential Mechanism for the Effects of Dexamethasone on Growth of Androgen-Independent Prostate Cancer</atitle><jtitle>JNCI : Journal of the National Cancer Institute</jtitle><addtitle>JNCI J Natl Cancer Inst</addtitle><date>2001-11-21</date><risdate>2001</risdate><volume>93</volume><issue>22</issue><spage>1739</spage><epage>1746</epage><pages>1739-1746</pages><issn>0027-8874</issn><eissn>1460-2105</eissn><coden>JNCIEQ</coden><abstract>Background: Dexamethasone, a synthetic glucocorticoid, has clinical benefit in patients with hormone-refractory prostate cancer (HRPC), but the mechanisms responsible for its effects are unknown. The nuclear factor-κB (NF-κB)-dependent cytokine interleukin (IL) 6 (IL-6) is thought to stimulate growth of HRPC. Because dexamethasone interferes with NF-κB activation, we determined whether dexamethasone inhibits prostate cancer growth by working through the glucocorticoid receptor (GR) to interfere with NF-κB–IL-6 pathway. Methods: Three human prostate cancer cell lines (DU145, PC-3, and LNCaP) were assessed for GR expression and responsiveness to dexamethasone. Levels of GR, NF-κβ, and the cytoplasmic NF-κβ inhibitor IκBα were determined by western blotting and of IL-6 by enzyme immunoassay. The subcellular localization of NF-κβ was analyzed by immunofluorescence. The effects of dexamethasone (thrice weekly injections of 1 μg/mouse) on DU145 xenografts in nude and severe combined immunodeficient (SCID) mice were evaluated. GR expression in human prostate cancers was assessed by immunohistochemistry. All statistical tests were two-sided. Results: Dexamethasone dose dependently decreased GR levels and inhibited the growth of DU145 and PC-3 but not LNCaP cells (DU145 cells, P<.001; PC-3 cells, P = .009). Dexamethasone increased IκBα protein levels and the cytosolic accumulation of NF-κB in DU145 cells and decreased secreted IL-6 levels to 37 pg/mL (95% confidence interval [CI] = 33 pg/mL to 41 pg/mL), compared with 164 pg/mL (95% CI = 162 pg/mL to 166 pg/mL) secreted by ethanol-treated control cells. Dexamethasone inhibited the growth of DU145 xenografts in nude (P = .006) and SCID (P = .026) mice without affecting GR levels. Eight of 16 human prostate cancers expressed GR at high levels (≥30% GR-positive cells). Conclusion: Dexamethasone inhibited the growth of GR-positive cancers, possibly through the disruption of the NF-κB–IL-6 pathway.</abstract><cop>Cary, NC</cop><pub>Oxford University Press</pub><pmid>11717335</pmid><doi>10.1093/jnci/93.22.1739</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0027-8874 |
| ispartof | JNCI : Journal of the National Cancer Institute, 2001-11, Vol.93 (22), p.1739-1746 |
| issn | 0027-8874 1460-2105 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_72295146 |
| source | Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Androgens - physiology Animals Biological and medical sciences Blotting, Western Cell Division - drug effects Dexamethasone - pharmacology DNA-Binding Proteins - metabolism Humans I-kappa B Proteins Interleukin-6 - metabolism Male Medical sciences Mice Mice, Nude Models, Animal Neoplasm Transplantation Nephrology. Urinary tract diseases NF-kappa B - metabolism NF-KappaB Inhibitor alpha Prostatic Neoplasms - metabolism Prostatic Neoplasms - pathology Receptors, Glucocorticoid - metabolism Reverse Transcriptase Polymerase Chain Reaction Transfection Transplantation, Heterologous - pathology Tumor Cells, Cultured Tumors of the urinary system Urinary tract. Prostate gland |
| title | Potential Mechanism for the Effects of Dexamethasone on Growth of Androgen-Independent Prostate Cancer |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-06T08%3A45%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Potential%20Mechanism%20for%20the%20Effects%20of%20Dexamethasone%20on%20Growth%20of%20Androgen-Independent%20Prostate%20Cancer&rft.jtitle=JNCI%20:%20Journal%20of%20the%20National%20Cancer%20Institute&rft.au=Nishimura,%20Kazuo&rft.date=2001-11-21&rft.volume=93&rft.issue=22&rft.spage=1739&rft.epage=1746&rft.pages=1739-1746&rft.issn=0027-8874&rft.eissn=1460-2105&rft.coden=JNCIEQ&rft_id=info:doi/10.1093/jnci/93.22.1739&rft_dat=%3Cproquest_cross%3E72295146%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=220977628&rft_id=info:pmid/11717335&rfr_iscdi=true |