• Title/Summary/Keyword: 암세포 증식억제 효과

Search Result 374, Processing Time 0.026 seconds

The Extract from Artemisia annua Linné. Induces p53-independent Apoptosis through Mitochondrial Signaling Pathway in A549 Lung Cancer Cells (A549 폐암세포에서 미토콘드리아 경로를 통한 개똥쑥 추출물의 apoptosis 유도 효과)

  • Kim, Bo-Min;Kim, Guen-Tae;Kim, Eun-Ji;Lim, Eun-Gyeong;Kim, Sang-Yong;Kim, Young-Min
    • Journal of Life Science
    • /
    • v.26 no.8
    • /
    • pp.887-894
    • /
    • 2016
  • The extract from Artemisia annuain L.(AAE) is known as a medicinal herb that is effective against cancer. Apoptosis is the process of programmed cell death, and mitochondria are known to play a central role in cell death control. In this study, we evaluated the p53-independent apoptosis of extract of AAE through downregulation of Bcl-2 and the mitochondrial pathway in A549 (lung cancer cells). AAE may exert cancer cell apoptosis through regulating p-Akt, Cox-2, p53 and mitochondria-mediated apoptotic proteins. p-Akt/cox-2 is known to play an important role in cell proliferation and cell survival. The Bcl-2 pro-apoptotic proteins (such as Bax, Bak and Bim) mediate the permeabilization of the mitochondrial outer membrane. Treatment of AAE reduces p-Akt, p-Mdm2, cox-2 and anti-apoptotic proteins (such as Bcl-2), while tumor suppressor p53 and pro-apoptotic proteins. Activation of Bax/Bak releases cytochrome c from mitochondria to the cytosol to activate a caspase. Caspase-3 is the major effector caspase associated with apoptotic pathways. Caspase-3 generally exists in cytoplasm in the form of a pro-enzyme. In the initiation stage of apoptosis, caspase-3 is activated by proteolytic cleavage and activated caspase-3 cleaves poly (ADP-ribose) polymerase (PARP). We treated Pifithrin-α (p53 inhibitor) and Celecoxib (Cox-2 inhibitor) to learn the relationship between the signal transduction of proteins associated with apoptosis. These results suggest that AAE induces apoptosis through a p53-independent pathway in A549.

Apoptotic Cell Death by Pectenotoxin-2 in p53-Deficient Human Hepatocellular Carcinoma Cells (종양억제유전자 p53 결손 인체간암세포에서 Pectenotoxin-2에 의한 Apoptosis 유도)

  • Shin, Dong-Yeok;Kim, Gi-Young;Choi, Byung-Tae;Kang, Ho-Sung;Jung, Jee-H.;Choi, Yung-Hyun
    • Journal of Life Science
    • /
    • v.17 no.10
    • /
    • pp.1447-1451
    • /
    • 2007
  • Through the screening of marine natural compounds that inhibit cancer cell proliferation, we previously reported that pectenotoxin-2 (PTX-2) isolated from marine sponges exhibits selective cytotoxicity against several cell lines in p53-deficient tumor cells compared to those with functional p53. However, the molecular mechanisms of its anti-proliferative action on malignant cell growth are not completely known. To further explore the mechanisms of its anti-cancer activity and to test whether the status of p53 in liver cancer cells correlates with their chemo-sensitivities to PTX-2, we used two well-known hepatocarcinoma cell lines, p53-deficient Hep3B and p53-wild type HepG2. We have demonstrated that PTX-2 markedly inhibits Hep3B cell growth and induces apoptosis whereas HepG2 cells are much more resistant to PTX-2 suggesting that PTX-2 seems to act by p53-independent cytotoxic mechanism. The apoptosis induced by PTX-2 in Hep3B cells was associated with the modulation of DNA fragmentation factor (DFF) family proteins, up-regulation of pro-apoptotic Bcl-2 family members such as Bax and Bcl-xS and activation of caspases (caspase-3, -8 and -9). Blockade of the caspase-3 activity by caspase-3 inhibitor, z-DEVD-fmk, prevented the PTX-2-induced growth inhibition in Hep3B cells. Moreover, treatment with PTX-2 also induced phosphorylation of AKT and extracellular-signal regulating kinase (ERK), but not c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MARK). Specific inhibitors of PI3K inhibitor (LY294002) and ERK1/2 inhibitor (PD98059) significantly blocks PTX-2-induced-anti-proliferative effects, whereas a JNK inhibitor (SP600125) and a p38 MAPK inhibitor (SB203580) have no significant effects demonstrating that the pro-apoptotic effect of PTX-2 mediated through activation of AKT and ERK signal pathway in Hep3B cells.

Voluntary Motor Control Change after Gait Training in Patients with Spinal Cord Injury (척수신경손상 환자의 보행훈련 전.후의 능동적 근육제어의 변화)

  • 임현균;이동철;이영신;셔우드아더
    • Journal of Biomedical Engineering Research
    • /
    • v.24 no.2
    • /
    • pp.133-140
    • /
    • 2003
  • In this study, muscle activity was measured using surface EMG (sEMG) during a voluntary maneuver (ankle dorsiflexion) in the supine position was compared pre and post gait training. Nine patients with incomplete spinal cord injury participated in a supported treadmill ambulation training (STAT), twenty minutes a day, five days a week for three months. Two tests, a gait speed test and a voluntary maneuver test, were made the same day, or at least the same week, pre and post gait training. Ten healthy subjects' data recorded using the same voluntary maneuvers were used for the reference. sEMG measured from ten lower limb muscles was used to observe the two features of amplitude and motor control distribution pattern, named response vector. The result showed that the average gait speed of patients increased significantly (p〈0.1) from 0.47$\pm$0.35 m/s to 0.68$\pm$0.52 m/s. In sEMG analysis, six out of nine patients showed a tendency to increase the right tibialis anterior activity during right ankle dorsiflexion from 109.7$\pm$148.5 $mutextrm{V}$ to 145.9$\pm$180.7 $mutextrm{V}$ but it was not significant (p〈0.055). In addition, only two patients showed increase of correlation coefficient and total muscle activity in the left fide during left dorsiflexion. Patients' muscle activity changes after gait training varied individually and generally depended on their muscle control abilities of the pre-STAT status. Response vector being introduced for quantitative analysis showed good Possibility to anticipate. evaluate, and/or guide patients with SCI, before and after gait training.

Antioxidant and Anticancer Activities of Extracts from Styela clava According to the Processing Methods and Solvents (가공방법 및 용매에 따른 미더덕 추출물의 항산화 및 항암효과)

  • Kim, Jin-Ju;Kim, Sun-Jung;Kim, Sun-Hee;Park, Hae-Ryong;Lee, Seung-Cheol
    • Journal of the Korean Society of Food Science and Nutrition
    • /
    • v.35 no.3
    • /
    • pp.278-283
    • /
    • 2006
  • Styela clava was processed by four different kinds of method including FR (fresh S. clava), H1 (heat treated S. clava at $110^{\circ}C$ for 15 min) H2 (heat treated S. clava at $120^{\circ}C$ for 5 min), and FD (freeze dried S. clava). Each S. clava sample was treated with methanol, ethanol, acetone, and water, then antioxidant and anticancer activities of the extracts were evaluated. In extracts from non-dried S. clava (FR, H1, and H2), total extract yield decreased with increasing treated temperature. The extraction yield was in the order of ethanol>methanol>water>acetone among treated solvents. In case of dried S. clava (FR), the extraction yield was lower than non-dried samples, and was in the order of methanol>ethanol>water>acetone. The radical scavenging activity (RSA) of non-dried S. clava (FR, H1, and H2) was in the order of acetone>ethanol>methanol and heat treatment also decreased RSA. RSA of FD was the highest in ethanol extract, while acetone and water extracts did not show RSA. When antioxidant activity was determined by reducing power (RD), methanol extract of FR showed the highest values and heat treatment decreased RD, too. RD of FD was in the order of methanol>ethanol>water>acetone. The acetone extracts from FD showed significant anticancer activity against human colon cancer cell line HT-29. These results indicated that extraction yield and properties of extracts from S. clava were dependent on processing temperature, solvent and/or physicochemical state. The appropriate extraction process should provide some valuable bioactive materials from S. clava.