• Korean Journal of Food Science and Technology
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• v.36 no.2
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• pp.339-344
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• 2004

Effects of 18 kinds of yuza extracts on viability of prostate cancer cells, DU 145 and LN-CaP, were investigated. Chloroform and methanolic extracts of yuza peel exhibited moderate cytotoxicity against both cancer cell lines dose-dependently and also showed antioxidant activity matching on inhibition of cell viability (author's intension not clear). Chloroform extract of yuza peel exhibited highest radical-scavenging activity and cytotoxicity against prostate cancer cells in vitro.

• Asian Pacific Journal of Cancer Prevention
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• v.16 no.3
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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.

• BMB Reports
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• v.50 no.9
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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.

• Biomolecules & Therapeutics
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• v.28 no.2
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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.

• Bulletin of the Korean Chemical Society
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• v.35 no.7
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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 ($IC_{50}=7.3{\mu}M$).

• BMB Reports
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• v.31 no.5
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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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.18 no.6
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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.

• Applied Microscopy
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• v.38 no.3
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• pp.245-250
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• 2008

Etoposide (Eto) is chemotherapeutic compounds that is currently used in the treatment of metastatic prostate cancer but new therapeutic agents are needed for the treatment of androgen-independent prostate cancer. The objective of the present study was to determine whether vitamin C (VC), the antioxidant, plays a role in regulating the growth of prostate cancer cell lines and whether VC has synergistic effect to tumor cell killing by chemotherapeutic drugs. Androgen-dependent LNCaP and androgen-independent DU-145 prostate cancer cell lines were used in this study. Both cells presented increase of dose- and time-dependent cytotoxicity in Eto-treated cultures. The combined treatment with Eto and VC significantly increased the percentage of apoptotic cells compared to Eto-treated cells(p<0.05). The present findings demonstrated that VC inhibited the growth of prostate cancer cell lines by Eto-mediated cytotoxicity and induced apoptosis. These results suggest that the chemotherapeutic effect of Eto on prostate cancer can be enhanced by VC.

• Biomolecules & Therapeutics
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• v.23 no.5
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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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.17 no.5
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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.