• Title/Summary/Keyword: anticancer activity and apoptosis

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Antioxidant and Anticancer Activities of Leaves Extracts from Acer tegmentosum

  • Eo, Hyun Ji;Park, Gwang Hun;Kim, Da Som;Kang, Yeongyeong;Park, Youngki
    • Korean Journal of Plant Resources
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    • v.33 no.6
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    • pp.551-557
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    • 2020
  • In this study, we were performed to elucidate the antioxidant and anticancer activity by leaves extracts from Acer tegmentosum (AT-L). In DPPH, ABTS radical scavenging activity, the AT-L revealed the high scavenging activity. Especially, the AT-L measured the highest ABTS radical scavenging activity, which is higher than ascorbic acid. The types of human cancer cells for evaluating the anticancer activity were colorectal cancer (SW480), prostate cancer (PC-3), breast cancer (MCF-7), pancreatic cancer (AsPC-1), lung cancer (A549) and liver cancer (HepG2). Human cancer cell viability was measured using MTT assay. Treatment of the AT-L decreased the cell viability and induced apoptosis in SW480 cells. These results suggest that extracts of the AT-L can be used as supplementary material for developing the natural antioxidant and anticancer drug for human cancer cells.

The various mechanisms of Korean traditional medicines for anti-cancer (한약의 다양한 항암기전)

  • Park, Yeong-Chul;Park, Yong-Ki;Lee, Sun-Dong
    • The Korea Journal of Herbology
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    • v.27 no.3
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    • pp.39-55
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    • 2012
  • Objectives : Recently there have been encouraging results, from a western perspective, in the cancer research field regarding the anticancer effects of herbal medicine. This paper was aimed to review herbal medicine playing its anticancer role in terms of apoptosis, inflammation control, differentiation and telomerase. Methods : New studies for tang, medicinal herb itself or effective ingradients of medicinal herb showing anti-cancer effectiveness were reviewed and summarized in terms of pharmacological action. Results : Ethanol extracts of $Spatholobus$ $suberectus$ greatly inhibited cancer cell growth inducing cell apoptosis and cytotoxic effects. $Scutellaria$ $baicalensis$ may be responsible for its anticancer activity showing inhibition of $PGE_2$ synthesis via suppression of COX-2 expression. Saikosaponins isolated from $Bupleurum$ induced the differentiation of C6 glioma cells, cancer cells, into astrocytes, normal cells. Acetone extract of $Bupleurum$ $scorzonerifolium$ inhibited proliferation of human lung cancer cells via inducing apoptosis and suppressing telomerase activity. Conclusions : Herbal medicine inhibited cancer cell growth inducing cell apoptosis and cytotoxic effects. Inflammation persisting for a decade eventually elevates the risk of cancer sufficiently that it is discernible in case control epidemiological studies. Differentiation therapy is defined as a therapy to treat cancers by inducing differentiation of the stem cells. Telomerase expression is a hallmark of cancer. Nearly the complete spectrum of human tumors has been shown to be telomerase positive.

Induction of ROS-dependent apoptosis by ethanol extract of Hizikia fusiforme in HT29 colon carcinoma cells (톳 에탄올 추출물에 의한 HT29 결장암 세포의 ROS 의존적 세포사멸 유도)

  • Su Hyun, Hong;Yung Hyun, Choi
    • Journal of Marine Bioscience and Biotechnology
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    • v.14 no.2
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    • pp.93-101
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    • 2022
  • Hizikia fusiforme, a type of brown algae, is widely used in Asian cuisine. It has been reported to have various pharmacological effects. In this study, the effects of the ethanol extract from H. fusiforme (EAHF) on the proliferation of human colon carcinoma cells were investigated. The effect on the survival of human hepatocarcinoma and colon carcinoma cells was examined, and results revealed that the anti-proliferative effects of EAHF were higher in colon carcinoma cells than in hepatocarcinoma cells. The inhibition of proliferation of HT29 colon carcinoma cells by EAHF treatment was closely related to the induction of apoptosis. EAHF treatment also increased caspase activity and poly(ADP-ribose) polymerase degradation, induced mitochondrial dysfunction, altered Bcl-2 family protein expression, and increased the rate of cytochrome c released from the mitochondria into the cytoplasm. Furthermore, the production of reactive oxygen species (ROS) was markedly stimulated by EAHF treatment, and when ROS production was blocked, EAHF-induced cytotoxicity was significantly attenuated. These results indicate that the anticancer activity of EAHF in HT29 colon carcinoma cells was induced by ROS-dependent mitochondrial impairment. While EAHF exhibited potent anticancer activity in colon carcinoma cells in this study, further studies on the active components of EAHF and their efficacy should be performed.

Antioxidative and Anticancer Activities of Julbernardia globiflora Extract in Human Colon Adenocarcinoma HT29 Cells (Julbernardia globiflora 추출물의 항산화 활성 및 인체 대장암 세포 HT29에 대한 항암 활성 분석)

  • Oh, You Na;Jin, Soojung;Kwon, Hyun Ju;Kim, Byung Woo
    • Journal of Life Science
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    • v.27 no.5
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    • pp.545-552
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    • 2017
  • Julbernardia globiflora, a tropical African tree widespread in Miombo woodland, has been used in folk medicine for the treatment of depression and stomach problems. However, the antioxidative and anticancer activities of J. globiflora remain unclear. The objective of this study is to evaluate the antioxidative and anticancer effects of methanol extract of J. globiflora (MEJG) and the molecular mechanism of its anticancer activity in human colon carcinoma HT29 cells. MEJG exhibited significant antioxidative effect with an $IC_{50}$ (concentration at 50% inhibition) value of $1.23{\mu}g/ml$ measuring by 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging assay and inhibited cell proliferation in a dose-dependent manner in HT29 cells. We found that MEJG induced apoptosis of HT29 cells with the increase of apoptotic cells and apoptotic bodies using Annexin V staining and 4,6-diamidino-2-phenylindole (DAPI) staining, respectively. The MEJG treatment showed the increase of Fas, a death receptor, and Bax, a pro-apoptotic protein, and the decrease of Bcl-2, an anti-apoptotic protein, resulting in the release of cytochrome c from the mitochondria into the cytosol and activation of caspase-3, -8 and -9. The apoptotic effects of MEJG were confirmed by cleavage of poly (ADP-ribose) polymerase (PARP). Collectively, these results suggest that MEJG may exert the anticancer effect in HT29 cells by inducing apoptosis via both the intrinsic and extrinsic pathways.

Screening of Anticancer Potential of Celecoxib and its Derivatives (셀레콕시브 및 그 합성유도체들의 항암활성 스크리닝)

  • Park, Jeong-Ran;Kang, Jin-Hyoung;Kuh, Hyo-Jeong;Noh, Ji-Young;Ryu, Hyung-Chul;Park, Sang-Wook;Ko, Dong-Hyun;Cho, Il-Hwan;Lee, Joo-Y.;Hwang, Daniel-H.;Kim, In-Kyung
    • Journal of Pharmaceutical Investigation
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    • v.33 no.2
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    • pp.105-112
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    • 2003
  • Selective COX (cyclooxygenase)-2 inhibitors including celecoxib have been shown to induce apoptosis and cell cycle changes in various tumor cells. New inhibitors are recently being developed as chemomodulating agents. We evaluated celecoxib and screened 150 synthetic compounds for anti-proliferative activities in vitro. Effects of celecoxib on COX activity, cell growth, cell cycle distribution, and apoptosis induction were determined in A549 COX-2 overexpressing human non-small cell lung cancer (NSCLC) cells. The COX inhibition of celecoxib increased with concentration up to 82% at $1\;{\mu}M$ after 24 hr exposure. Forty ${\mu}M$ and $50\;{\mu}M$ of ce1ecoxib induced $G_1$ arrest, and TUNEL-positive apoptotic cells, respectively. Among 150 compounds, several compounds were selected for having greater COX-2 inhibitory activity and higher selectivity than celecoxib with growth inhibitory activity. Celecoxib showed concentration-dependent COX inhibitory activity, and ability to induce cell cycle arrest and apoptosis in human NSCLC cells in vitro. Among synthetic analogues screened, several compounds showed promising in vitro activity as COX-2 inhibitory anticancer agents, which warrant further evaluation in vitro and in vivo.

Anticancer Effects and Mechanisms of Co-Treatment of Cisplatin with Taurine in MCF-7 Cells (MCF-7에서 Cisplatin과 타우린의 병용처리로 인한 항암효과 및 관련 기전)

  • Kim, Taehee;Kim, An Keun
    • YAKHAK HOEJI
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    • v.57 no.1
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    • pp.18-23
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    • 2013
  • The objective of this study is to evaluate the synergic effects of combined treatment with taurine and cisplatin in human breast cancer, MCF-7 cells. For this study, MCF-7 cells were treated with taurine (5, 10, and 20 mM) and cisplatin (0.5 ${\mu}M$) for 48 and 72 hrs. Co-treatment of cisplatin with taurine decreased cell proliferation more compared with cisplatin alone. Reduced cell proliferation was caused by apoptosis. Therefore we investigated the apoptotic cells. After treatment of cisplatin and taurine, apoptotic cells were slightly increased. Apoptosis-related proteins, cleaved caspases and cytochrome c were increased. The present study suggests that combination treatment of cisplatin with taurine enhance anticancer activity of cisplatin in MCF-7 cells.

Induction of Apoptosis by Scolopendra subspinipes mutilans in Human Leukemia HL-60 Cells through Bcl-xL Regulation (왕지네(Scolopendra subspinipes mutilans)의 Bcl-xL 조절에 의한 HL-60 세포의 아폽토시스(Apoptosis) 유도)

  • Kim, Kil-Nam;Kim, Sang-Bum;Yoon, Weon-Jong;Yang, Kyoung-Sik;Park, Soo-Yeong
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.37 no.11
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    • pp.1408-1414
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    • 2008
  • The anticancer properties of Scolopendra subspinipes mutilans extract were investigated. The extract from S. subspinipes mutilans by 80% EtOH was fractionated with n-hexane, dichloromethan ($CH_2Cl_2$), ethylacetate (EtOAc), and butanol (BuOH) in order. The EtOAc fraction showed the highest inhibitory activity (about 80%) against human leukemia (HL-60) cell growth at $50\;{\mu}g/mL$. To explore the mechanism of cytotoxicity, we used several measures of apoptosis to determine whether these processes were involved in EtOAc fraction-induced HL-60 cell death. Our results showed EtOAc fraction induced cell shrinkage, cell membrane blebbing, apoptotic body, and DNA fragmentation. The EtOAc fraction gradually decreased the expression of anti-apoptotic Bcl-xL and led to the activation of caspase-3, -9 and cleavage of PARP. These findings suggest that S. subspinipes mutilans exhibits potential anticancer properties.

Auranofin accelerates spermidine-induced apoptosis via reactive oxygen species generation and suppression of PI3K/Akt signaling pathway in hepatocellular carcinoma

  • Hyun Hwangbo;Da Hye Kim;Min Yeong Kim;Seon Yeong Ji;EunJin Bang;Su Hyun Hong;Yung Hyun Choi;JaeHun Cheong
    • Fisheries and Aquatic Sciences
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    • v.26 no.2
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    • pp.133-144
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    • 2023
  • Auranofin is a US Food and Drug Administration (FDA)-approved anti-arthritis medication that functions as a thioredoxin reductase inhibitor. Spermidine, a polyamine present in marine algae, can exert various physiological functions. Herein, we examined the synergistic anticancer activity of auranofin and spermidine in hepatocellular carcinoma (HCC). Combined treatment with auranofin and spermidine suppressed cell viability more efficiently than either treatment alone in HCC Hep3B cells. The isobologram plotted by calculating the half maximal inhibitory concentration (IC50) values of each drug indicated that the two drugs exhibited a synergistic effect. Based on the analysis of annexin V and cell cycle distribution, auranofin and spermidine markedly induced apoptosis in Hep3B cells. Moreover, auranofin and spermidine increased mitochondria-mediated apoptosis by promoting mitochondrial membrane potential (Δψm) loss. Auranofin and spermidine significantly increased reactive oxygen species (ROS) production in Hep3B cells, and the blocking ROS suppressed apoptosis induced by spermidine and auranofin. In addition, auranofin and spermidine reduced the expression of phosphorylated phosphatidylinositol-3 kinase (PI3K) and protein kinase B (Akt), and PI3K inhibitor accelerated auranofin- and spermidine-induced apoptosis. Using ROS scavenger and PI3K inhibitor, we revealed that ROS acts upstream of auranofin- and spermidine-induced apoptosis. Collectively, our study suggests that combination treatment with auranofin and spermidine could afford synergistic anticancer activity via ROS overproduction and reduced PI3K/Akt signaling pathway.

Effects of Oxidative Stress on Apoptosis and Antioxidant Enzyme Levels

  • Kim, Choonmi;Lee, Ji-Young
    • Biomolecules & Therapeutics
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    • v.4 no.4
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    • pp.402-407
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    • 1996
  • Effects of oxidative stress on the induction of apoptosis and the activity of antioxidant enzymes were investigated in HL-60 cells using $H_2O$$_2$and cisplatin which generate oxygen species in the cell. Various concentrations of oxidants were treated to cells and at different incubation time, cells were harvested for assays. Cell viability, morphology by propidium iodide staining and DNA fragmentation by agarose gel electrophoresis were observed to determine whether they induce apoptosis. The activity of antioxidant enzymes such as superoxide dismutase and catalase was also measured to evaluate the cellular response to the oxidative damage. The results are as follows: $H_2O$$_2$ induced apoptosis at 10 $\mu$M after 6h incubation, while it took 12h for cisplatin. Both oxidants induced the superoxide dismutase activity at a tolerable low concentration. However, at a concentration which causes apoptotic cell death, the enzyme level was dropped markedly at first and then recovered to the normal level after which it declined again, probably due to cell death. On the other hand, changes in the activity of catalase were not significant at most concentrations except the statistically significant decrease at 24h after 10 $\mu$M-$H_2O$$_2$treatment. In this study, $H_2O$$_2$- and cisplatintreated cells showed similar results in apoptotic response and enzyme activities, suggesting that anticancer activity of cisplatin may be related, at least in part, to the production of oxygen free radicals.

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Combined Treatment with Coptidis Rhizoma Extract and Arsenic Trioxide Enhanced Apoptosis through Diverse Pathways in H157 Cells

  • Youn, Myung-Ja;Kim, Yun-Ha;Kim, Hyung-Jin;Song, Je-Ho;Jeon, Ho-Sung;Yu, Dong-Hee;Sul, Jeong-Dug;So, Hong-Seob;Park, Rae-Kil
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.23 no.6
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    • pp.1449-1459
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    • 2009
  • Coptidis rhizoma (huanglian) is an herb that is widely used in traditional Chinese medicine that has recently been shown to possess anticancer activity. However, the molecular mechanism underlying the anticancer effects of this herb is poorly understood. In this study, we investigated the anticancer activity of a combination of CR extract and arsenic trioxide, as well as the apoptotic pathway associated with its mechanism of action in human lung cancer H157 cells. Combined treatment of H157 cells with CR extract and arsenic trioxide resulted in significant apoptotic death. In addition, combined treatment with CR extract and arsenic trioxide acted in concert to induce a loss of mitochondrial membrane potential (${\Delta}{\Psi}$), the release of cytochrome c from mitochondria, and an increase in the expression of pro-apoptotic p53 and Bax protein, which resulted in activation of caspases and apoptosis. CR extract combined with arsenic trioxide also increased the lipid peroxidation, mRNA expression of DR4 and DR5 and caspase-8 activity. These data indicate that combined treatment with CR extract and arsenic trioxide enhanced apoptotic cell death in H157 cells through diverse pathways, including mitochondrial dysfunction and death receptors, particularly DR4 and DR5. Thus, this treatment may be an effective from of chemotherapy.