• 한국융합학회논문지
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• 제13권2호
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• pp.257-262
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• 2022

본 연구의 목적은 다양한 생리활성물질을 함유한 비트 추출물의 다양한 농도를 이용하여 인체 유래 암세포 증식 저해를 살펴보기 위하여 실시하였다. 실험에 사용한 인체 유래 암세포는 6종으로 전립샘암세포 DU145, 폐암세포 A549, 유방암세포 MCF-7, 자궁암세포 HeLa, 간암세포 SNU-182, 담도암세포 SNU-1196을 사용하였으며, 비트 추출물의 다양한 농도에 대한 암세포증식 저해를 CCK-8 방법으로 측정하였다. 암세포증식 저해를 살펴본 결과 비트 추출물은 전립샘암세포 DU145를 모든 농도에서 유의성있게 농도 의존적으로 저해하였으며, 폐암세포 A549, 전립샘암세포 DU-145는 100ug/mL, 1000ug/mL에서 자궁암세포 HeLa, 간암세포 SNU-182, 담도암세포 SNU-1196는 1000ug/mL에서 유의한 증식 저해를 보였다. 실험 결과, 다양한 인체 유래 암세포를 이용한 비트 추출물의 암세포증식 저해는 암 예방 효과 및 기능성 식품 개발의 가능성을 제공한다고 볼 수 있다.

• Biomolecules & Therapeutics
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• 제21권1호
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• pp.10-20
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• 2013

Prostate cancer is one of the most prevalent non-skin related cancers. It is the second leading cause of cancer deaths among males in most Western countries. If prostate cancer is diagnosed in its early stages, there is a higher probability that it will be completely cured. Prostatic acid phosphatase (PAP) is a non-specific phosphomonoesterase synthesized in prostate epithelial cells and its level proportionally increases with prostate cancer progression. PAP was the biochemical diagnostic mainstay for prostate cancer until the introduction of prostate-specific antigen (PSA) which improved the detection of early-stage prostate cancer and largely displaced PAP. Recently, however, there is a renewed interest in PAP because of its usefulness in prognosticating intermediate to high-risk prostate cancers and its success in the immunotherapy of prostate cancer. Although PAP is believed to be a key regulator of prostate cell growth, its exact role in normal prostate as well as detailed molecular mechanism of PAP regulation is still unclear. Here, many different aspects of PAP in prostate cancer are revisited and its emerging roles in other environment are discussed.

• Biomolecules & Therapeutics
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• 제13권3호
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• pp.185-189
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• 2005

We isolated a coumarin compound, isoimperatorin ($C_{16}H_{14}O_4$ mw: 270) from Angelica koreana through silica gel column chromatography, and characterized it by NMR. Here, for the first time we observed that isoimperatorin (25, 50 and 100 ${\mu}M$) treatment for 24-72h inhibited growth and induced death in human prostate carcinoma DU145 cells. Further, in mechanistic investigation, isoimperatorin-induced cell growth inhibition was associated with a strong increase in G1 arrest in cell cycle progression, which started at 24h of the treatment. These findings suggest a novel anticancer efficacy of isoimperatorin mediated via induction of G1 arrest against hormone refractory human prostate carcinoma DU145 cells.

• Applied Microscopy
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• 제38권3호
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• pp.245-250
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• 2008

전립선암은 남성 사망의 주된 원인이 되는 치명적인 질병으로 남성호르몬 의존형과 비의존형이 있다. Etoposide (Eto)는 현재 전립선암을 치료하는 데 사용하고 있으나 남성호르몬 비의존형에는 치료 성공률이 낮아서, 보다 효과적인 치료제 개발이 절실히 요구되어왔다. 본 연구는 항산화제인 vitamin C (VC)가 전립선 암세포에 어떠한 역할을 하는지 알아보고자 남성호르몬 의존형-전립선 암세포인 LNCaP와 비의존형 암세포인 DU-145에 비교적 낮은 농도의 Eto와 VC를 복합처리한 결과, Eto만을 투여한 것과 비교하여 암세포의 성장이 현저하게 억제되었고, apoptosis의 발생률 역시 유의적으로 증가하였다(p<0.05). 이러한 결과는 VC가 전립선암 치료제로 사용하고 있는 Eto의 효과를 증가시킬 수 있음을 강력히 시사하는 것이다.

• Bulletin of the Korean Chemical Society
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• 제33권1호
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• pp.111-114
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• 2012

Androgen receptor (AR) is ligand-inducible nuclear hormone receptor which has been focused on key molecular target in growth and progression of prostate cancer. We synthesized a series of 4-aryl 2-substituted aniline-thiazole analogs and evaluated their anti-cancer activity in AR-dependent human prostate cancer LNCap cells. Among them, the compound 6 inhibited the tumor growth in LNCap-inoculated xenograft model.

• Asian Pacific Journal of Cancer Prevention
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• 제15권5호
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• pp.2179-2183
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• 2014

Background: In vitro, in vivo and clinical studies have demonstrated anti-cancer effects of deuterium depleted water (DDW). The nature of this agents action, cytotoxic or cytostatic, remains to be elucidated. We here aimed to address the point by examining effects on different cell lines. Materials and Methods: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) -based cytotoxicity analysis was conducted for human breast, stomach, colon, prostate cancer and glioblastoma multiforme cell lines as well as human dermal fibroblasts. The cell lines were treated with decreasing deuterium concentrations of DDW alone, paclitaxel alone and both. One way analysis of variance (ANOVA) was used for statistical analysis. Results: Treatment with different deuterium concentrations of DDW alone did not impose any significant inhibitory effects on growth of cell lines. Paclitaxel significantly decreased the survival fractions of all cell lines. DDW augmented paclitaxel inhibitory effects on breast, prostate, stomach cancer and glioblastoma cell lines, with influence being more pronounced in breast and prostate cases. Conclusions: DDW per se does not appear to have inhibitory effects on the assessed tumor cell lines as well as normal fibroblasts. As an adjuvant, however, DDW augmented inhibitory effects of paclitaxel and thus it could be considered as an adjuvant to conventional anticancer agents in future trials.

• Toxicological Research
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• 제26권2호
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• pp.109-115
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• 2010

The purpose of this study was to elucidate the mechanism underlying enhanced radiosensitivity to $^{60}Co\;{\gamma}$-irradiation in human prostate PC-3 cells pretreated with berberine. The cytotoxic effect of the combination of berberine and irradiation was superior to that of berberine or irradiation alone. Cell death and Apoptosis increased significantly with the combination of berberine and irradiation. Additionally, ROS generation was elevated by berberine with or without irradiation. The antioxidant NAC inhibited berberine and radiation-induced cell death. Bax, caspase-3, p53, p38, and JNK activation increased, but activation of Bcl-2, ERK, and HO-1 decreased with berberine treatment with or without irradiation. Berberine inhibited the anti-apoptotic signal pathway involving the activation of the HO-1/NF-${\kappa}B$-mediated survival pathway, which prevents radiation-induced cell death. Our data demonstrate that berberine inhibited the radioresistant effects and enhanced the radiosensitivity effects in human prostate cancer cells via the MAPK/caspase-3 and ROS pathways.

• 대한동의생리학회:학술대회논문집
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• 대한동의생리학회 2005년도 정기총회 및 동계학술대회
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• pp.30-30
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• 2005

• Asian Pacific Journal of Cancer Prevention
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• 제14권6호
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• pp.3499-3502
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• 2013

MicroRNAs (miRNAs) are a class of endogenously expressed small, non-coding, single-stranded RNAs that negatively regulate gene expression, mainly by binding to 3'- untranslated regions (3'UTR) of their target messenger RNAs (mRNAs), which cause blocks of translation and/or mRNA cleavage. Recently, miRNAprofiling studies demonstrated the microRNA-497 (miR-497) level to be down-regulated in all prostate carcinomas compared with BPH samples. The purpose of this study was to investigate the potential role of miR-497 in human prostate cancer. Proliferation, cell cycle and apoptosis assays were conducted to explore the potential function of miR-497 in human prostate cancer cells. Results showed that miR-497 suppressed cellular growth and initiated G0/G1 phase arrest of LNCaP and PC-3 cells. We also observed that miR-497 increased the percentage of apoptotic cells by increasing caspase-3/7 activity. Taken together, our results demonstrated that miR-497 can inhibit growth and induce apoptosis by caspase-3 activation in prostate cancer cells, which suggest its use as a potential therapeutic target in the future.

• BMB Reports
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• 제44권8호
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• pp.547-552
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• 2011

MED19 is a member of the Mediator that plays a key role in the activation and repression of signal transduction or the regulation of transcription in carcinomas. To tested the functional role of MED19 in human prostate cancer, we downregulated MED19 expression in prostate cancer cells (PC-3 and DU145) by lentivirus-mediated short hairpin (shRNA), and analyzed the effect of inhibition of MED19 on prostate cancer cell proliferation and tumorigenesis. The in vitro prostate cancer cell proliferation, colony formation, and in vivo tumor growth in nude mice xenografts was significantly reduced after the downregulation of MED19. Knockdown of MED19 caused S-phase arrest and induced apoptosis via modulation of Bid and Caspase 7. It was suggested that MED19 serves as a novel proliferation regulator that promotes growth of prostate cancer cells.