• Journal of Ginseng Research
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• v.40 no.1
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• pp.62-67
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• 2016

Background: Ginseng, which is widely used in functional foods and as an herbal medicine, has been reported to reduce the proliferation of prostate cancer cells by mechanisms that are not yet fully understood. Methods: This study was designed to investigate the changes in ginsenoside content in ginseng after treatment with a microwave-irradiation thermal process and to verify the anticancer effects of the extracts. To confirm the anticancer effect of microwave-irradiated processed ginseng (MG), it was tested in three human prostate cancer cell lines (DU145, LNCaP, and PC-3 cells). Involvements of apoptosis and autophagy were assessed using Western blotting. Results: After microwave treatment, the content of ginsenosides Rg1, Re, Rb1, Rc, Rb2, and Rd in the extracts decreased, whereas the content of ginsenosides 20(S)-Rg3, 20(R)-Rg3, Rk1, and Rg5 increased. Antiproliferation results for the human cancer cell lines treated with ginseng extracts indicate that PC-3 cells treated with MG showed the highest activity with an half maximal inhibitory concentration of $48{\mu}g/mL$. We also showed that MG suppresses the growth of human prostate cancer cell xenografts in athymic nude mice as an in vivo model. This growth suppression by MG is associated with the inductions of cell death and autophagy. Conclusion: Therefore, heat processing by microwave irradiation is a useful method to enhance the anticancer effect of ginseng by increasing the content of ginsenosides Rg3, Rg5, and Rk1.

• YAKHAK HOEJI
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• v.43 no.3
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• pp.369-377
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• 1999

A new series of highly water soluble platinum(II) complexes {Pt(II)[1,3-bis(phenylthio) propane](trans- -1,2-diaminocyclohexane) (PC-1) and Pt(II)[1,3-bis-(phenythio)propane] cis-1,2-diaminocyclohexane(PC-2)} were synthesized, and characterized by their elemental analysis and by various spectroscopic techniques[infrared(IR), 13C-nuclear magnetic resonance (NMR)]. In vitro antitumor activity of new Pt(II) complexes was tested against P-388 and L-1210 mouse lymphocytic leukemia cell lines, PC-14 / P, PC-14/ADM and PC-14 / CDDP human pulmonary adenocarcinima, DU-145 human prostate carcinoma, HT-1376 human bladder carcinoma, ZR-75-1 human breast carcinoma, MKN-45/P and MKN-45/CDDP human gastric adenocarcinoma cell lines using colorimetric MTT[3-(4,5-dimethyl thiazol-2-yl)-2.5-diphenyltetrazoliumbromide] assay for cell survival and proliferation. PC-1 showed active against L-1210, P-388 leukemia, human lung, stomach, prostate, bladder and breast cancer cell lines, and the antitumor activity of these compounds were comparable or superior to those of PC-2 and displatin. The nephrotoxicities of PC-1 and PC-2 were found quite less than that of cisplatin using MTT and [3H] thymidine uptake in rabbit proximal tubule cells and human kidney cortical cells. Based on these results, this novel platinum (II) complex compound (PC-1) represents a valuable lead in the development of a new anticancer chemotherapeutic agent capable of improving antitumor activity and low nephrotoxicity.

• 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 ($IC_{50}=7.3{\mu}M$).

• Journal of Life Science
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• v.18 no.8
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• pp.1042-1048
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• 2008

Prostate cancer is the most predominant cancer in men and related death rate increases every year. Till date, there is no effective therapy for androgen independent prostate cancer. To investigate the mechanism for cell growth inhibition or apoptosis in human androgen independent prostate cancer PC-3 cells after gamma irradiation. The aim of this study was to examine the potential of gamma irradiation to induce apoptosis in PC-3 cells and to assess the mechanism of gamma irradiation-induced apoptosis. Five different assays were employed in this study: cell proliferation assay, morphological assessments of apoptotic cells, DNA fragmentation analysis, quantification of apoptosis by annexin V (AV) and propidium iodide (PI) staning, and western blot analysis. Cell viability was inversely related to radiation dose. DAPI-positive cells were detected 48 hr after 40 Gy radiation exposure. And nuclear morphological changes of cells were observed by gamma irradiation. DNA ladder patterns in the cells exposed to gamma-radiation were appeared at 24 hr. Also, gamma irradiation induces apoptosis of PC-3 cells via Caspase3, Bax and PARP-dependent fashion.

• The Korea Journal of Herbology
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• v.27 no.4
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• pp.17-23
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• 2012

Objectives : Schisandrae Fructus (SF) has traditionally been used to balance level of body fluid and to strengthen kidney function. It has been reported that the SF extract has antioxidant, hepatoprotective, neuroprotective and anticancer effects. This study investigated an antiproliferative effect of SF extract on PC-3 human prostate cancer cells and analyzed active ingredients of SF extract qualitatively and quantitatively. Methods : We examined the antiproliferative effect of SF extract with MTT assay, DAPI staining and annexin-V/7-AAD double staining. The active ingredients of SF extract were identified by using HPTLC and HPLC/DAD system. Results : SF-chloroform fraction inhibited growth of PC-3 cells and changed the morphology of nucleus in a dose dependent manner. A dose-dependent apoptotic cell death was also measured by flow cytometry analysis. It was analyzed that SF-chloroform fraction contained more schizandrin than other fractions by using HPTLC and HPLC/DAD system. Conclusions : These results suggest that SF extract and schizandrin may be a potential chemotherapeutic agent for the control of PC-3 human prostate cancer cells.

• Toxicological Research
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• v.22 no.1
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• pp.31-37
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• 2006

It was previously found that melittin inhibited $NF-{\kappa}B$ activity by reacting with signal molecules of $NF-{\kappa}B$ which is critical contributor in cancer cell growth by induction of apoptotic cell death. We here investigated whether melittin inhibits cell growth of human prostate cancer cells through induction of apoptotic cell death, and the possible signal pathways. Melittin ($0{\sim}1\;{\mu}g/ml$) inhibited prostate cancer cell growth in a dose dependent manner. Conversely related to the growth inhibitory effect, melittin increased the induction of apoptotic cell death in a dose dependent manner. Melittin also inhibited DNA binding activity of $NF-{\kappa}B$, an anti-apoptotic transcriptional factor. Consistent with the induction of apoptotic cell death and inhibition of $NF-{\kappa}B$, melittin increased the expression of pro-apoptotic proteins caspase-3, and Bax but down-regulated anti-apoptotic protein Bcl-2. These findings suggest that melittin could inhibit prostate cancer cell growth, and this effect may be related with the induction of apoptotic cell death via inactivation of $NF-{\kappa}B$.

• Journal of Life Science
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• v.26 no.4
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• pp.398-405
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• 2016

Statins, the inhibitors of 3-hydroxy 3-methylglutaryl coenzyme A (HMG-CoA) reductase, are widely used in treatments of hypercholesterolemia and newly known as anti-cancer effect of various cancer cells. Recently, several studies suggested that reactive oxygen species (ROS) play a critical role on cell death signaling. However, mechanism of ROS by rosuvastatin is currently unclear. This study aimed to explore the molecular mechanism of apoptosis by rosuvastatin in human prostate cancer PC-3 cells. Cell viability and apoptosis-related protein expression were measured by MTT assay and western blotting, respectively. In addition, the levels of apoptosis and ROS were analyzed. The results showed that rosuvastatin dramatically reduced cell viability in a dose- and time-dependent manner. We confirmed that rosuvastatin induced apoptosis through reduction of procaspase-3 and cleavage of poly (ADP-ribose) polymerase (PARP) in PC-3 cells. In addition, rosuvastatin stimulated ROS production in a dose-dependent manner and pre-treatment with N-acetylcysteine (NAC), a ROS scavenger, significantly recovered rosuvastatin-induced ROS and apoptosis. Thus, we concluded that rosuvastain induces apoptosis through generation of ROS in human prostate cancer PC-3 cells and provides a promising approach to improve the efficacy of cancer therapy.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.12
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• pp.6369-6374
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• 2012

Vitexicarpin (3', 5-dihydroxy-3, 4', 6, 7-tetramethoxyflavone), a polymethoxyflavone isolated from Viticis Fructus (Vitex rotundifolia Linne fil.), has long been used as an anti-inflammatory herb in traditional Chinese medicine. It has also been reported that vitexicarpin can inhibit the growth of various cancer cells. However, there is no report elucidating its effect on human prostate carcinoma cells. The aim of the present study was to examine the apoptotic induction activity of vitexicarpin on PC-3 cells and molecular mechanisms involved. MTT studies showed that vitexicarpin dose-dependently inhibited growth of PC-3 cells with an $IC_{50}{\sim}28.8{\mu}M$. Hoechst 33258 staining further revealed that vitexicarpin induced apoptotic cell death. The effect of vitexicarpin on PC-3 cells apoptosis was tested using prodium iodide (PI)/Annexin V-FITC double staining and flow cytometry. The results indicated that vitexicarpin induction of apoptotic cell death in PC-3 cells was accompanied by cell cycle arrest in the G2/M phase. Furthermore, our study demonstrated that vitexicarpin induction of PC-3 cell apoptosis was associated with upregulation of the proapoptotic protein Bax, and downregulation of antiapoptotic protein Bcl-2, release of Cytochrome c from mitochondria and decrease in mitochondrial membrane potential. Our findings suggested that vitexicarpin may become a potential leading drug in the therapy of prostate carcinoma.

• Nutrition Research and Practice
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• v.1 no.3
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• pp.195-199
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• 2007

Inositol hexaphosphate ($IP_6$) is a major constituent of most cereals, legumes, nuts, oil seeds and soybean. Previous studies reported the anticancer effect of $IP_6$ and suggested that co-treatment of $IP_6$ with inositol may enhance anticancer effect of $IP_6$. Although the anticancer effect of $IP_6$ has been intensively studied, the combinational effect of $IP_6$ and inositol and involved mechanisms are not well understood so far. In the present study, we investigated the effect of $IP_6$ and myo-inositol (MI) on cell cycle regulation and apoptosis using PC3 prostate cancer cell lines. When cell, were co-treated with $IP_6$ and MI, the extent of cell growth inhibition was significantly increased than that by $IP_6$ alone. To identify the effect of $IP_6$ and MI on apoptosis, the activity of caspase-3 was measured. The caspase-3 activity was significantly increased when cells were treated with either $IP_6$ alone or both $IP_6$ and MI, with no significant enhancement by co-treatment. To investigate the effect of $IP_6$ and MI of cell cycle arrest, we measured p21 mRNA expression in PC3 cells and observed significant increase in p21 mRNA by $IP_6$. But synergistic regulation by co-treatment with $IP_6$ and MI was not observed. In addition, there was no significant effect by co-treatment compared to $IP_6$ treatment on the regulation of cell cycle progression although $IP_6$ significantly changed cell cycle distribution in the presence of MI or not. Therefore, these findings support that $IP_6$ has anticancer function by induction of apoptosis and regulation of cell cycle. However, synergistic effect by MI on cell cycle regulation and apoptosis was not observed in PC3 prostate cancer cells.

• Toxicological Research
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• v.26 no.2
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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.