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Docetaxel 내성 전립선암세포주에 대한 Trichostatin A의 항암효과
이영주(Young Ju Lee),연재승(Jae Seung Yeon),김성한(Sung Han Kim),이은식(Eunsik Lee),변석수(Seok Soo Byun),이상철(Sang Chul Lee),정창욱(Chang Wook Jeong),홍성규(Sung Kyu Hong),이상은(Sang Eun Lee) 대한비뇨기종양학회 2012 대한비뇨기종양학회지 Vol.10 No.2
Purpose: To determine anti-tumor effect of a histone deacetylase (HDAC) inhibitor, trichostatin A (TSA) in docetaxel- resistant human prostate cancer cells (PC3DR2). Materials and Methods: PC3DR2 was established from the PC3 prostate cancer cell line by continuous exposure to escalating concentrations of docetaxel. PC3 and PC3DR2 were exposed to escalating dose of TSA and tumor cell proliferation was examined by Cell Counting Kit-8 (CCK-8) assay. To evaluate the changes in cell cycle and apoptosis, flow cytometry was used and clonogenic assay was performed. Expression of cIAP1, PARP, caspase-3, and caspase-8 were analyzed by Western blot analysis. Results: Acute TSA administration (0-2μM for 24-72 hours) suppressed tumor cell proliferation in a timeand dose-dependent manner (p<0.05) in both prostate tumor cell lines. TSA with 0.2μM concentration induced G2/M phase cell cycle arrest in PC3 but not in PC3DR2 cell lines. A significant decrease in colony number was seen with the TSA treatment in the two cell lines. Western blot analysis revealed down-regulated cIAP1 and up-regulated PARP, caspase 8 and caspase 3 with the increasing concentrations of TSA in both cell lines. Conclusions: PC3DR2 was established and our results suggest anti-tumor effect of TSA in inhibiting PC3DR2 through its proapoptotic effect.
Cis-platin 내성 방광암세포주에 대한 Trichostatin A의 항암효과 분석
박지현(Jihyun Park),변석수(Seok-Soo Byun),이정은(Jeong Eun Lee),오종진(Jong Jin Oh),이상철(Sang Chul Lee),홍성규(Sung Kyu Hong),윤철용(Cheol Yong Yoon),이은식(Eunsik Lee),이상은(Sang Eun Lee) 대한비뇨기종양학회 2011 대한비뇨기종양학회지 Vol.9 No.2
Purpose: To determine anti-tumor effect of a histone deacetylase (HDAC) inhibitor, trichostatin A (TSA) in cis-platin resistant human bladder cancer cells (T24R2). Materials and Methods: T24 bladder cancer cell line and T24R2 were exposed to escalating dose of TSA and tumor cell proliferation was examined by CCK-8 assay. To evaluate the changes in cell cycle and apoptosis, flow cytometry was used and clonogenic assay was performed. Expression of p21WAF1/CIP1, cIAP1, XIAP, Bcl-2, and Bax were analyzed by Western blot. Results: Acute TSA administration (0.1-2μM for 24-72hours) suppressed tumor cell proliferation in a time- and dose-dependent manner (p<0.05) in all two bladder tumor cell lines. TSA induced G1 phase cell cycle arrest in both bladder cell lines and higher-fraction of sub-G1 (apoptotic portion) with 0.5μM in T24R2. A significant decrease in colony number was seen with the TSA treatment in the two cell lines. Western blot analysis revealed up-regulated p21 and bax, and down-regulated bcl-2, cIAP1 and xIAP with the increasing concentrations of TSA in both cell lines. Conclusions: Our results suggest anti-tumor effect of TSA in inhibiting bladder cancer growths and its potential role as an agent for treating cisplatin-resistant bladder cancer.
정창욱(Chang Wook Jeong),변석수(Seok-Soo Byun),이은식(Eunsik Lee),이상은(Sang Eun Lee),정병하(Byung Ha Chung),최영득(Young Deuk Choi),최한용(Han Yong Choi),이현무(Hyun Moo Lee),안한종(Hanjong Ahn),황태곤(Tae-Kon Hwang),이강현(Kang Hy 대한비뇨기종양학회 2013 대한비뇨기종양학회지 Vol.11 No.3
Purpose: Previously, Seoul National University (SNU) prostate cancer (PC) stage calculator was developed to predict the pathological stage of clinically localized PC after radical prostatectomy (RP) in Korean men. We evaluated its generalizability and compared their clinical values with 2013 Partin tables by Korean multicenter cohort. Materials and Methods: Evaluated cohort consisted of 2,607 patients who had clinical stages T1c-T3a PC and were treated with RP at 14 institutions in Korea. After excluding 262 cases with prior hormone or radiation therapy and 604 cases with missing data, 1,741 cases were analyzed. Predictive accuracy was evaluated using the area under the receiver operating characteristic curve (AUC). The agreement between the predicted values with observed outcome was assessed with calibration plot. SNU PC stage calculator was compared with 2013 Partin tables applying to this cohort using DeLong method and decision curve analysis. Results: The accuracies of SNU PC stage calculator was all higher than those of 2013 Partin tables to predict organ-confined disease (0.755 vs. 0.711, p<0.001), extraprostatic extension (0.743 vs. 0.665, p<0.001), seminal vesicle invasion (0.833 vs. 0.764, p<0.001), and lymph node metastasis (0.842 vs 0.760, p=0.019). The observed outcomes were well calibrated with their predicted values by the calculator. Decision curve analyses demonstrated higher net benefits of SNU PC stage calculator compared with 2013 Partin tables.