• 제목/요약/키워드: DU145 prostate cancer cell

검색결과 54건 처리시간 0.023초

In vitro 상에서 유자(Citrus junos SIEB ex TANAKA) 용매 추출물의 암세포 억제효과 및 항산화성 (In Vitro Effect of Yuza (Citrus junos SIEB ex TANAKA) Extracts on Proliferation of Human Prostate Cancer Cells and Antioxidant Activity)

  • 유경미;황인경
    • 한국식품과학회지
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    • 제36권2호
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    • pp.339-344
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    • 2004
  • 유자는 성숙할수록 과피와 과육의 총페놀 함량은 많아지고 자유기 소거능이 높아지는 경향을 보였다. 유자로부터 추출한 18가지 용매 추출물의 항산화 활성과 전립선 암세포 DU 145, LN-CaP에 대한 세포독성 실험을 실시한 결과 과피와 과육 모두 미성숙한 유자 보다 성숙한 후 수확한 유자가 그 활성이 높게 나타냈다. 용매별로 살펴보면 과성숙 유자 과피, 과육의 클로로포름, 메탄올 추출물은 전립선 암세포 DU 145에 대하여 60% 이상의 세포사멸 효과를 나타났으며 메탄올 추출물의 효과도 농도에 따라 상당히 높은 것으로 나타났다. 또한 세포 조직을 현미경으로 살펴본 결과 추출물의 처리 농도가 증가할수록 세포 사멸이 쉽게 이루어지는 것을 확인 할 수 있었다. 이런 세포 사멸의 경향은 추출물의 자유기 소거 환성이 높을수록 높게 나타났다.

Short Low Concentration Cisplatin Treatment Leads to an Epithelial Mesenchymal Transition-like Response in DU145 Prostate Cancer Cells

  • Liu, Yi-Qing;Zhang, Guo-An;Zhang, Bing-Chang;Wang, Yong;Liu, Zheng;Jiao, Yu-Lian;Liu, Ning;Zhao, Yue-Ran
    • Asian Pacific Journal of Cancer Prevention
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    • 제16권3호
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    • pp.1025-1028
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    • 2015
  • Background: Prostate cancer is one of the main causes of cancer death, and drug resistance is the leading reason for therapy failure. However, how this occurs is largely unknown. We therrfore aimed to study the response of DU145 cells to cisplatin. Materials and Methods: Du145 prostate cancer cells were treated with a low dose of cisplatin for 24 h and cell viability and number were determined by MTT assay and trypan blue exclusion assay, respectively. The real time polymerase chain reaction (PCR) was used to assess responses to cisplatin treatment. Results: After 24h $2{\mu}g/ml$ treatment did not result in significant reduction in cell viability or number. However, it led to enhanced cancer cell invasiveness. E-cadherin mRNA was reduced, and vimentin, Snail, Slug, metalloproteinase 9 (MMP9) mRNA expression increased significantly, a feature of epithelial-mesenchymal transition (EMT). Conclusions: Short time low concentration cisplatin treatment leads to elevated invasiveness of DU145 cancer cells and this is possibly due to EMT.

Identification of simvastatin-regulated targets associated with JNK activation in DU145 human prostate cancer cell death signaling

  • Jung, Eun Joo;Chung, Ky Hyun;Kim, Choong Won
    • BMB Reports
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    • 제50권9호
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    • pp.466-471
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    • 2017
  • The results of this study show that c-Jun N-terminal kinase (JNK) activation was associated with the enhancement of docetaxel-induced cytotoxicity by simvastatin in DU145 human prostate cancer cells. To better understand the basic molecular mechanisms, we investigated simvastatin-regulated targets during simvastatin-induced cell death in DU145 cells using two-dimensional (2D) proteomic analysis. Thus, vimentin, Ras-related protein Rab-1B (RAB1B), cytoplasmic hydroxymethylglutaryl-CoA synthase (cHMGCS), thioredoxin domain-containing protein 5 (TXNDC5), heterogeneous nuclear ribonucleoprotein K (hnRNP K), N-myc downstream-regulated gene 1 (NDRG1), and isopentenyl-diphosphate Delta-isomerase 1 (IDI1) protein spots were identified as simvastatin-regulated targets involved in DU145 cell death signaling pathways. Moreover, the JNK inhibitor SP600125 significantly inhibited the upregulation of NDRG1 and IDI protein levels by combination treatment of docetaxel and simvastatin. These results suggest that NDRG1 and IDI could at least play an important role in DU145 cell death signaling as simvastatinregulated targets associated with JNK activation.

A New Histone Deacetylase Inhibitor, MHY4381, Induces Apoptosis via Generation of Reactive Oxygen Species in Human Prostate Cancer Cells

  • Richa, Sachan;Dey, Prasanta;Park, Chaeun;Yang, Jungho;Son, Ji Yeon;Park, Jae Hyeon;Lee, Su Hyun;Ahn, Mee-Young;Kim, In Su;Moon, Hyung Ryong;Kim, Hyung Sik
    • Biomolecules & Therapeutics
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    • 제28권2호
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    • pp.184-194
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    • 2020
  • Histone deacetylase (HDAC) inhibitors represent a novel class of anticancer agents, which can be used to inhibit cell proliferation and induce apoptosis in several types of cancer cells. In this study, we investigated the anticancer activity of MHY4381, a newly synthesized HDAC inhibitor, against human prostate cancer cell lines and compared its efficacy with that of suberoylanilide hydroxamic acid (SAHA), a well-known HDAC inhibitor. We assessed cell viability, apoptosis, cell cycle regulation, and other biological effects in the prostate cancer cells. We also evaluated a possible mechanism of MHY4381 on the apoptotic cell death pathway. The IC50 value of MHY4381 was lower in DU145 cells (IC50=0.31 µM) than in LNCaP (IC50=0.85 µM) and PC-3 cells (IC50=5.23 µM). In addition, the IC50 values of MHY4381 measured in this assay were significantly lower than those of SAHA against prostate cancer cell lines. MHY4381 increased the levels of acetylated histones H3 and H4 and reduced the expression of HDAC proteins in the prostate cancer cell lines. MHY4381 increased G2/M phase arrest in DU145 cells, and G1 arrest in LNCaP cells. It also activated reactive oxygen species (ROS) generation, which induced apoptosis in the DU145 and LNCaP cells by increasing the ratio of Bax/Bcl-2 and releasing cytochrome c into the cytoplasm. Our results indicated that MHY4381 preferentially results in antitumor effects in DU145 and LNCaP cells via mitochondria-mediated apoptosis and ROS-facilitated cell death pathway, and therefore can be used as a promising prostate cancer therapeutic.

Synthesis of New 4-(tert-Octyl)phenol Derivatives and Their Anticancer Activity against Human Prostate and Lung Cancer Cell Lines

  • Che, Haiyan;Fang, Yuanying;Gurung, Santosh K.;Luo, Jun;Yoon, Deok Hyo;Sung, Gi-Ho;Kim, Tae Woong;Park, Haeil
    • Bulletin of the Korean Chemical Society
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    • 제35권7호
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    • pp.2038-2042
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    • 2014
  • 4-(tert-Octyl)phenol derivatives bearing the D-mannitol substructure (6a, 6b, 7) were prepared from $\small{D}$-mannitol and evaluated their anticancer activity against human lung (A549) and prostate (Lncap, Du145, PC3) cancer cell lines. Among derivatives tested, the bis(tert-octyl)phenoxy compound 7 exhibited strongest proliferation inhibitory activities against human cancer cell lines tested, especially high sensitivity to human Du145 prostate cancer cells ($IC_{50}=7.3{\mu}M$).

Conditioned Media of ASC-17D Sertoli Cells Induce G1-Growth Arrest of DU145 Human Prostate Cancer Cells

  • Kang, Hyeog;Kang, Sang-Wook;Choi, Sang-Hyun;Lee, Kwang-Ho;Chun, Boe-Gwun;Min, Bon-Hong
    • BMB Reports
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    • 제31권5호
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    • pp.508-514
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    • 1998
  • We studied the effects of ASC-17D rat Sertoli cell-conditioned media (rSCCM) on the proliferation of the DU145 prostate cancer cells. rSCCM was prepared from ASC-17D cells cultured in DMEM/F-12 serum-free media at a nonpermissive temperature of $40^{\circ}C$, which is the condition for the high expression of c1usterin. We found that rSCCM could inhibit the proliferation of DU145 cells by arresting the cell cycle in the G1 phase in a dose-dependent manner. This growth arresting activity was abolished by boiling rSCCM for 5 min. The G1 growth-inhibiting activity of rSCCM was also detected in other prostate-originated cancer cells examined (i.e., LNCaP and PC-3) but not in other cells (ASC-17D, HepG2, SK-N-SH, and NIH3T3). Western blot analysis of partially purified growth inhibiting fractions with the clusterin antibody showed that the cytostatic factor in rSCCM was not c1usterin. This cytostatic factor was semi purified by DEAE-Sepharose, ammonium sulfate precipitation, and Phenyl-Sepharose column chromatography, and was estimated to have a molecular weight of 88 kDa by Sephacryl S-300 gel filtration.

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백작약 추출물의 전립선 암세포 고사 유도 효과 및 기전 연구 (Study on Apoptosis-Inducing Effects and Mechanism of Radix Paeoniae Alba Extract in DU145 Human Prostate Cancer Cell)

  • 권강범;김은경;김경종;강길성;김영선;김인규;김인섭;김인수;이수경;서은아;류도곤
    • 동의생리병리학회지
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    • 제18권6호
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    • pp.1617-1621
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    • 2004
  • The aim of this study was to investigate the apoptotic effect and its mechanism on Radix Paeoniae Alba Extract(RPAE) in DU145 human prostate cancer cell line. RPAE induced apoptosis in a dose-dependent manner in DU145 cells as confirmed by both discontinuous DNA fragmentation using Hoechst33342 staining and poly-(ADP-ribose) polymerase(PARP) cleavage, which are apoptotic signs. To clarify the mechanisms on RPAE-induced apoptosis, we examined the p50(NF-κB subunit), IκBα, PTEN and Par-4 protein expression using Western blotting. Treatment with RPAE resulted in the decrease of p50 expression by IκBα increase, which resulted in Par-4 increase and bcl-2 decrease in DU145 cells. These results suggest that apoptosis of DU145 cells by RPAE involved decreases of NF-κB activation and bcl-2 expression, increase of Par-4 protein expression.

Vitamin C+etoposide 복합투여에 의한 전립선 암세포 성장 억제의 상승 효과 (Vitamin C Enhances the Effect of Etoposide to Inhibit Human Prostate Cancer Growth in vitro)

  • 이명선
    • 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.

A New Histone Deacetylase Inhibitor, MHY219, Inhibits the Migration of Human Prostate Cancer Cells via HDAC1

  • De, Umasankar;Kundu, Soma;Patra, Nabanita;Ahn, Mee Young;Ahn, Ji Hae;Son, Ji Yeon;Yoon, Jung Hyun;Moon, Hyung Ryoung;Lee, Byung Mu;Kim, Hyung Sik
    • Biomolecules & Therapeutics
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    • 제23권5호
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    • pp.434-441
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    • 2015
  • Histone deacetylase (HDAC) inhibitors are considered novel agents for cancer chemotherapy. We previously investigated MHY219, a new HDAC inhibitor, and its potent anticancer activity in human prostate cancer cells. In the present study, we evaluated MHY219 molecular mechanisms involved in the regulation of prostate cancer cell migration. Similar to suberanilohydroxamic acid (SAHA), MHY219 inhibited HDAC1 enzyme activity in a dose-dependent manner. MHY219 cytotoxicity was higher in LNCaP ($IC_{50}=0.67{\mu}M$) than in DU145 cells ($IC_{50}=1.10{\mu}M$) and PC3 cells ($IC_{50}=5.60{\mu}M$) after 48 h of treatment. MHY219 significantly inhibited the HDAC1 protein levels in LNCaP and DU145 cells at high concentrations. However, inhibitory effects of MHY219 on HDAC proteins levels varied based on the cell type. MHY219 significantly inhibited LNCaP and DU145 cells migration by down-regulation of matrix metalloprotease-1 (MMP-1) and MMP-2 and induction of tissue inhibitor of metalloproteinases-1 (TIMP-1). These results suggest that MHY219 may potentially be used as an anticancer agent to block cancer cell migration through the repression of MMP-1 and MMP-2, which is related to the reduction of HDAC1.

인체 전립선 암세포에서 참나무 목초액에 의한 세포주기 S기 arrest 유발에 관한 연구 (Induction of S phase Arrest of the Cell Cycle by Oak Smoke Flavoring (Holyessing) in Human Prostate Carcinoma Cells)

  • 박철;이원호;최병태;김경철;이용태;최영현
    • 동의생리병리학회지
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    • 제17권5호
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    • pp.1309-1314
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    • 2003
  • We examined the effects of Oak Smoke Flavoring (OSF, Holyessing) on the cell proliferation of DU145 and PC3 human prostate carcinoma cell line. OSF treatment resulted in a concentration-dependent inhibition of the cell viability in both DU145 and PC3 cell lines. The anti-proliferative effects by OSF treatment in DU145 and PC3 cells were associated with morphological changes such as membrane shrinking and cell rounding up. DNA flow cytometric histograms showed that population of S phase of the cell cycle was increased by OSF treatment in a dose-dependent manner. Western blot analysis revealed that cyclin B1 and cdc2 proteins were reduced by OSF treatment in DU145 cells, whereas cyclin A was markedly inhibited in PC3 cells. Furthermore, we observed an increase of Cdk inhibitor p16 and p27 protein, and an inhibition of phosphorylation of pRB by OSF treatment in a dose-dependent manner. The present results indicated that OSF-induced inhibition of human prostate carcinoma cell proliferation is associated with the blockage of S phase progression.