https://scholars.lib.ntu.edu.tw/handle/123456789/541997
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.author | Altuwaijri S. | en_US |
dc.contributor.author | Wu C.-C. | en_US |
dc.contributor.author | Niu Y.-J. | en_US |
dc.contributor.author | Mizokami A. | en_US |
dc.contributor.author | HONG-CHIANG CHANG | en_US |
dc.contributor.author | Chang C. | en_US |
dc.creator | Altuwaijri S.;Wu C.-C.;Niu Y.-J.;Mizokami A.;Hong-Chiang Chang;Chang C. | - |
dc.date.accessioned | 2021-01-26T02:27:54Z | - |
dc.date.available | 2021-01-26T02:27:54Z | - |
dc.date.issued | 2007 | - |
dc.identifier.issn | 1008-682X | - |
dc.identifier.uri | https://www.scopus.com/inward/record.uri?eid=2-s2.0-33947269319&doi=10.1111%2fj.1745-7262.2007.00258.x&partnerID=40&md5=72a88e5673f8d03123ea09c24d620a0e | - |
dc.identifier.uri | https://scholars.lib.ntu.edu.tw/handle/123456789/541997 | - |
dc.description.abstract | Aim: To examine the physiological role of the androgen receptor (AR) in the PC-3 cell line by transfecting full-length functional AR cDNA driven by its natural human AR promoter. Methods: We generated an AR-expressing PC-3(AR)9 stable clone that expresses AR under the control of the natural human AR promoter and compared its proliferation to that of the PC-3(AR)2 (stable clone that expresses AR under the control of the cytomegalovirus (CMV) promoter, established by Heisler et al.) after androgen treatment. Results: We found that dihydrotestosterone (DHT) from 0.001 nmol/L to 10 nmol/L induces cell cycle arrest or inhibits proliferation of PC-3(AR)2 compared with its vector control, PC-3(pIRES). In contrast, PC-3(AR)9 cell growth slightly increased or did not change when treated with physiological concentrations of 1 nmol/L DHT. Conclusion: These data suggest that intracellular control of AR expression levels through the natural AR promoter might be needed for determining AR function in androgen-independent prostate cancer (AIPC) PC-3 cells. Unlike previous publications that showed DHT mediated suppression of PC-3 growth after transfection of viral promoter-driven AR overexpression, we report here that DHT-mediated PC-3 proliferation is slightly induced or does not change compared with its baseline after reintroducing AR expression driven by its own natural promoter, as shown in PC-3(AR)9 prostate cancer cells. ? 2007 Asian Journal of Andrology, Shanghai Institute of Materia Medica, Chinese Academy of Sciences. | - |
dc.relation.ispartof | Asian Journal of Andrology | - |
dc.subject | Androgen ablation therapy; Androgen receptor; Apoptosis; Proliferation; Prostate cancer | - |
dc.subject.classification | [SDGs]SDG3 | - |
dc.subject.other | androgen; androgen receptor; androstanolone; complementary DNA; androgen independent prostate cancer cell; apoptosis; article; cancer cell; cell clone; cell cycle arrest; cell growth; cell proliferation; controlled study; Cytomegalovirus; human; human cell; male; promoter region; prostate cancer; protein expression; protein function; Cell Cycle; Cell Line, Tumor; Cell Proliferation; Dihydrotestosterone; DNA, Complementary; Humans; Male; Promoter Regions (Genetics); Prostatic Neoplasms; Receptors, Androgen; Transfection | - |
dc.title | Expression of human AR cDNA driven by its own promoter results in mild promotion, but not suppression, of growth in human prostate cancer PC-3 cells | en_US |
dc.type | journal article | en |
dc.identifier.doi | 10.1111/j.1745-7262.2007.00258.x | - |
dc.identifier.pmid | 17334587 | - |
dc.identifier.scopus | 2-s2.0-33947269319 | - |
dc.relation.pages | 181-188 | - |
dc.relation.journalvolume | 9 | - |
dc.relation.journalissue | 2 | - |
item.openairetype | journal article | - |
item.openairecristype | http://purl.org/coar/resource_type/c_6501 | - |
item.fulltext | no fulltext | - |
item.grantfulltext | none | - |
item.cerifentitytype | Publications | - |
crisitem.author.dept | Urology-NTUH | - |
crisitem.author.orcid | 0000-0001-5411-6680 | - |
crisitem.author.parentorg | National Taiwan University Hospital | - |
顯示於: | 醫學系 |
在 IR 系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。