Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이철훈 | - |
dc.date.accessioned | 2019-04-16T05:06:13Z | - |
dc.date.available | 2019-04-16T05:06:13Z | - |
dc.date.issued | 2016-01 | - |
dc.identifier.citation | ANTICANCER RESEARCH, v. 36, No. 1, Page. 213-220 | en_US |
dc.identifier.issn | 0250-7005 | - |
dc.identifier.issn | 1791-7530 | - |
dc.identifier.uri | http://ar.iiarjournals.org/content/36/1/213.full | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/102082 | - |
dc.description.abstract | Background: Previously, we synthesized a new carbocyclic analog of pyrrolo[2,3-d]pyrimidine nucleoside, designated MCS-C3. Recently, we found that LNCaP androgen-responsive prostate cancer cells treated with MCS-C3 rapidly undergo intrinsic apoptosis through dramatic up-regulation of p21(CIP1). The present study aimed to evaluate the cellular functions and underlying molecular mechanisms of p21(CIP1) on apoptotic induction in LNCaP cells treated with 6 mu M MCS-C3. Materials and Methods: Western blots, flow cytometric assay, immunoprecipitation, and transmission electron microscopy analysis were used to measure apoptotic induction in 6-mu M MCS-C3-treated LNCaP cells. Effects of MCS-C3 on gene expression of p21(CIP1) were measured by semi-quantitative real-time polymerase chain reaction, and small interfering RNA transfection. Results: MCS-C3 induced appreciable caspase-dependent apoptosis associated with the significant up-regulation of p53-dependent p21(CIP1) in LNCaP cells. Moreover, this apoptotic induction was caused by direct binding of p21(CIP1) to anti-apoptotic B-cell lymphoma 2 (BCL2) protein, and antagonizing BCL2 function. In addition, MCS-C3-mediated apoptotic induction, and up-regulation of p21(CIP1) were almost completely blocked by the treatment of androgen-esponsive LNCaP cells with flutamide, an androgen receptor (AR) antagonist. Conclusion: We identified that induction of intrinsic apoptosis in LNCaP cells by 6 mu M MCS-C3 is associated not only with p53 activation but also with mediation of AR. In the present study, we identified the cellular functions and underlying molecular mechanisms of p53-dependent and AR-associated p21(CIP1) on apoptotic induction via direct binding to BCL2 in LNCaP cells treated with 6 mu M MCS-C3. | en_US |
dc.description.sponsorship | This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Korean government (MSIP) (2013R1A1A2011531). | en_US |
dc.language.iso | en_US | en_US |
dc.publisher | INT INST ANTICANCER RESEARCH | en_US |
dc.subject | Prostate cancer | en_US |
dc.subject | LNCaP cells | en_US |
dc.subject | apoptosis | en_US |
dc.subject | p21(CIP1) | en_US |
dc.subject | BCL2 | en_US |
dc.subject | ANDROGEN RECEPTOR | en_US |
dc.subject | P21 | en_US |
dc.subject | EXPRESSION | en_US |
dc.subject | P53 | en_US |
dc.subject | INDUCTION | en_US |
dc.subject | MITOCHONDRIA | en_US |
dc.subject | SANGIVAMYCIN | en_US |
dc.subject | ASSOCIATION | en_US |
dc.subject | INHIBITOR | en_US |
dc.subject | CLEAVAGE | en_US |
dc.title | p21(CIP1) Induces Apoptosis via Binding to BCL2 in LNCaP Prostate Cancer Cells Treated with MCS-C3, A Novel Carbocyclic Analog of Pyrrolopyrimidine | en_US |
dc.type | Article | en_US |
dc.relation.no | 1 | - |
dc.relation.volume | 36 | - |
dc.relation.page | 213-220 | - |
dc.relation.journal | ANTICANCER RESEARCH | - |
dc.contributor.googleauthor | Choi, Ko-Woon | - |
dc.contributor.googleauthor | Suh, Hyewon | - |
dc.contributor.googleauthor | Oh, Ha Lim | - |
dc.contributor.googleauthor | Ryou, Chongsuk | - |
dc.contributor.googleauthor | Lee, Chul-Hoon | - |
dc.relation.code | 2016001814 | - |
dc.sector.campus | E | - |
dc.sector.daehak | COLLEGE OF PHARMACY[E] | - |
dc.sector.department | DEPARTMENT OF PHARMACY | - |
dc.identifier.pid | chhlee | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.