• 대한본초학회지
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• 제21권4호
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• pp.51-58
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• 2006

Objectives : In this study, we investigate that Ulmi cortex extract contributes to growth inhibitory effect and anti-cancer activity on the HT-29 human colon cancer cells. Methods : Ulmi cortex was extracted from the leaves of the plant using water. The Ulmi cortex extract was treated to different concentrations for 24 hr. Growth inhibitory effect was analyzed by measuring FACS study and MTT assay. Cell cycle inhibition was confirmed by kinases assay. Cell apoptosis was confirmed by surveying caspases cascades activation using Western blot. Results : Exposure to Ulmi cortex extract (0.4mg/ml) results in an inhibitory effect on cell growth in HT-29 cells. Growth inhibition by Ulmi cortex extract in HT-29 cells was related with the inhibition of proliferation and induction of apoptosis. The Ulmi cortex extract induces G1-cell cycle arrest and DNA fragmentation in HT-29 cells. Furthermore, Ulmi cortex extract induces cell apoptosis through the activation of caspases-3 and PARP cleavage. Conclusion : Ulmi cortex extract induces apoptosis in human colon cancer cells, therefore, we suggest that Ulmi cortex extract can be used as a novel class of anti-cancer drugs.

• 동의생리병리학회지
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• 제20권3호
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• pp.701-709
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• 2006

The Rhus verniciflua Stokes (乾漆-RVS) has been used in traditional East Asia medicine for the therapy of gastritis, stomach cancer, although the mechanism for the biological activity is unclear. In the present study aims to investigate RVS extract contributes to growth inhibitory effect and it's the molecular mechanism on the human gastric cancer cells. AGS (gastric cancer cells) and RIEI (normal cells) were treated to different concentrations and periods of RVS extract $(10{\;}{\sim{{\;}100{\;}ug/mil)$. Growth inhibitory effect was analyzed by measuring FACS study and MTS assay. Cell cycle inhibition was confirmed by measuring CDK2 kinase activity by immunoprecipitation and kinase assay. And apoptosis was confirmed by surveying caspase cascades activation using a pan caspase inhibitor Exposure to RVS extract (50 ug/mll) resulted in a synergistic inhibitory effect on cell growth in AGS cells. Growth inhibition was related with the inhibition of proliferation and induction of apoptosis. The extract induces Gl -cell cycle arrest through the regulation of cyclins, the induction of p27kip1, and the decrease CDK2 kinase activity. And upregulated p27kip1 level is caused by protein stability increment by the reduction of S-phase kinase-associated protein 2 (Skp2), a key molecule related with p27kip1 ubiquitination and degradation, and do novo protein synthesis. Besides, 乾漆 extract induces apoptosis through the expression of Bax, poly(ADP-ribose) polymerase (PARP) and activation of caspase-3. RVS extract induces Gl -cell cycle arrest via accumulation of p27kip1 and apoptosis in human gastric cancer cells but not in normal cells, therefore we suggest that the extract can be used as a novel class of anti-cancer drugs.

• Tuberculosis and Respiratory Diseases
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• 제75권1호
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• pp.9-17
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• 2013

Background: In cancer cells, autophagy is generally induced as a pro-survival mechanism in response to treatment-associated genotoxic and metabolic stress. Thus, concurrent autophagy inhibition can be expected to have a synergistic effect with chemotherapy on cancer cell death. Monensin, a polyether antibiotic, is known as an autophagy inhibitor, which interferes with the fusion of autophagosome and lysosome. There have been a few reports of its effect in combination with anticancer drugs. We performed this study to investigate whether erlotinib, an epidermal growth factor receptor inhibitor, or rapamycin, an mammalian target of rapamycin (mTOR) inhibitor, is effective in combination therapy with monensin in non-small cell lung cancer cells. Methods: NCI-H1299 cells were treated with rapamycin or erlotinib, with or without monensin pretreatment, and then subjected to growth inhibition assay, apoptosis analysis by flow cytometry, and cell cycle analysis on the basis of the DNA contents histogram. Finally, a Western blot analysis was done to examine the changes of proteins related to apoptosis and cell cycle control. Results: Monensin synergistically increases growth inhibition and apoptosis induced by rapamycin or erlotinib. The number of cells in the sub-$G_1$ phase increases noticeably after the combination treatment. Increase of proapoptotic proteins, including bax, cleaved caspase 3, and cleaved poly(ADP-ribose) polymerase, and decrease of anti-apoptotic proteins, bcl-2 and bcl-xL, are augmented by the combination treatment with monensin. The promoters of cell cycle progression, notch3 and skp2, decrease and p21, a cyclin-dependent kinase inhibitor, accumulates within the cell during this process. Conclusion: Our findings suggest that concurrent autophagy inhibition could have a role in lung cancer treatment.

• Journal of Microbiology and Biotechnology
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• 제17권11호
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• pp.1848-1855
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• 2007

Antibacterial activity of essential oils (Tea tree, Chamomile, Eucalyptus) on Staphylococcus aureus growth was evaluated as well as the essential oil-loaded alginate beads. The binding interactions between the cell and the essential oils were measured using an optical biosensor. The antibacterial activity of the essential oils to the cell was evaluated with their binding interaction and affinity. The antibacterial activity appeared in the order of Tea Tree>Chamomile>Eucalyptus, in comparison of the inhibition effects of the cell growth to the essential oils. The association rate constant and affinity of the cell binding on Tea Tree essential oil were $5.0{\times}10^{-13}\;ml/(CFU{\cdot}s)$ and $5.0{\times}10^5\;ml/CFU$, respectively. The affinity of the cell binding on Tea Tree was about twice higher than those on the other essential oils. It might be possible that an effective antibacterial activity of Tea Tree essential oil was derived from its strong adhesive ability to the cell, more so than those of the other essential oils.

• BMB Reports
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• 제48권10호
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• pp.565-570
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• 2015

In several reports, the respiratory syncytial virus (RSV) was identified as an oncolytic virus in cancer cells (e.g., lung and prostate cancer). However, the effects of RSV in hepatocellular carcinoma (HCC) cells have not yet been investigated. Here, we observed the inhibitory effects of RSV infection in HCC cell-lines. Cell growth was significantly decreased by RSV infection in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. After RSV infection, plaque formation and syncytial formation were observed in affected Hep3B and Huh-7 cells. RSV protein-expression was also detected in Hep3B and Huh-7 cells; however, only Huh-7 cells showed apoptosis after RSV infection. Furthermore, inhibition of cell migration by RSV infection was observed in BNL-HCC, Hep3B, Huh-7 and SNU-739 cells. Therefore, further investigation is required to clarify the molecular mechanism of RSV-mediated inhibition of HCC cell growth, and to develop potential RSV oncolytic viro-therapeutics.

• Archives of Pharmacal Research
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• 제20권6호
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• pp.572-578
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• 1997

To gain further insight into how antiestrogens modulate cell function, the effects of antiestrogen on cell proliferation were studied in human breast cancer cells. We examined the effects of trans-tamoxifen on the proliferation of three human breast cancer cell lines that differed in their estrogen receptor contents. Trans-tamoxifen $(1{\mu}M)$ markedly inhibited the estrogen stimulated proliferation of MCF-7 human breast cancer cells that contained high levels of estrogen receptor $(1.15{\pm}0.03 pmole/mg protein)$ over that of control. In T47D cells that contained low levels of estrogen receptor $(0.23{\pm}0.05 pmole/mg protein)$, trans-tamoxifen $(1{\mu}M)$ showed minimal inhibition of estrogen stimulated cell proliferation over that of control. MDA-MB-231 cells, that contained no detectable levels of estrogen receptors, had their growth unaffected by trans-tamoxifen treatment. These results showed their sensitivity to growth inhibition by antiestrogen conrrelated well with their estrogen receptor content. Also we examined the effect of antiestrogen on cellular progestrone receptor level as well as plasminogen activator activity in MCF-7 cells. Trans-tamoxifen $(1{\mu}M)$ showed maximal inhibition of estrogen stimulated progestrone receptor level as well as plasminogen activator activity in MCF-7 cells that were stimulated by estrogen. It is not clear whether these inhibitions of progestrone receptor and plasminogen activator activity by estrogen are related to the antiestrogen inhibition of cell proliferation of MCF-7 cells. From the results of this study, it is clearly demonstrated that trans-tamoxifen is an antiestrogen in MCF-7 human breast cancer cells. Our data suggest that the biological effectiveness of trans-tamoxifen appear to result from its affinity of interaction with the estrogen receptor.

• Journal of Acupuncture Research
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• 제23권2호
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• pp.47-59
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• 2006

We previously found that cobrotoxin 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 cobrotoxin inhibits cell growth of human prostate cancer cells through induction of apoptotic cell death, which is related with the suppression of the $NF-{\kappa}B$ activity. Cobrotoxin $(0{\sim}8\;nM)$ inhibited prostate cancer cell growth through increased apoptosis in a dose dependent manner. Cobrotoxin inhibited DNA binding activity of $NF-{\kappa}B$, an anti-apoptotic transcriptional factor. Consistent with the induction of apoptosis and inhibition of $NF-{\kappa}B$, cobrotoxin increased the expression of pro-apoptotic proteins caspase 3. Cobrotoxin, a venom of Vipera lebetina turanica, is a group of basicpeptides composed of 233 amino acids with six disulfide bonds formed by twelve cysteins. NF-kB is activated by subsequent release of inhibitory IkB and translocation of p50. Since sulfhydryl group is present in kinase domain of p50 subunit of NF-kB, cobrotoxin could modify NF-kB activity by protein-protein interaction. And Cobrotoxin down regulated Akt signals. Salicylic acid as a reducing agent of Sulf-hydryl group and LY294002 as a Akt inhibitor abrogated cobrotoxin-induced cell growth and DNA binding activity of $NF-{\kappa}B$. These findings suggest that nano to pico molar range of cobrotoxin could inhibit prostate cancer cell growth, and the effect may be related with the induction of apoptotic cell death through Akt dependent inhibition of $NF-{\kappa}B$ signal.

• 동의생리병리학회지
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• 제18권4호
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• pp.1147-1152
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• 2004

To investigate the anti-cancer effects of aqueous extract of Cheonkumwikyung-tang (CKWKT) on the growth of human lung carcinoma cell line A549, we performed various biochemical experiments such as the effects of CKWKT on the cell proliferation and viability, the morphological changes, the effects on expression of apoptosis and cell growth-regulatory gene products. Results obtained are as follow; CKWKT treatment declined the cell viability and proliferation of A549 cells in a concentration-dependent manner. The anti-proliferative effect by CKWKT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. CKWKT treatment induced apoptotic cell death of A549 cells in a concentration-dependent manner, which was associated with inhibition and/or degradation of apoptotic target proteins such poly(ADP-ribose) polymerase, β-catenin and phospholipase C-γ1. Western blot analysis revealed that the levels cyclin-dependent kinase inhibitor p21 expression were induced by CKWKT treatment in A549 cells. Taken together, these findings suggest that CKWKT-induced inhibition of human lung cancer cell proliferation is associated with the induction of apoptotic cell death via regulation of several major growth regulatory gene products and CKWKT may have therapeutic potential in human lung cancer.

• Ecology and Resilient Infrastructure
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• 제9권3호
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• pp.183-193
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• 2022

초음파 (ultrasonic) 조사시간 (irradiation time)에 따른 Microcystis aeruginosa (M. aeruginosa)의 성장억제 (growth inhibition) 효과를 대용량 (10 L) 조류 시료를 활용해 다양한 초음파 조사시간 동안 (0.5, 1, 1.5, 2, 2.5, 3 hr) 실험실 규모 (lab-scale) 실험을 진행하였다. Chl-a와 M. aeruginosa 개체수 (cell number) 분석 결과, 초음파 조사 종료 이후 모든 실험군에서 Chl-a와 개체수가 감소되어 조류 성장억제가 관찰되었으며, 초음파 조사시간이 2시간 미만인 실험군 (T_B, T_C, T_D)은 저감 이후 조류의 급격한 재성장 (regrowth)이 관측되었으나, 조사시간이 2시간 이상인 실험군 (T_E, T_F, T_G)은 2시간 미만 조사한 실험군 대비 조류성장억제가 1 - 2일 더 지속되는 것을 확인하였다. 또한, 조류의 개체수가 초기 개체수까지 회복 시간 (recovery time)을 검토한 결과 조사시간 2시간을 기준으로 실험군 T_B (0.5 hr)는 7일, T_C (1 hr)와 T_D (1.5 hr)는 약 20일, T_E, T_F, T_G (≥ 2 hr)는 약 30일이 소요되어 초음파 조사 종료 후 초기 개체수까지의 회복 시간의 차이를 확인하였다. 비성장속도 (𝜇)와 일차분해속도(𝜅)를 도출한 결과, 실험군은 성장억제 기간 동안 초음파 조사시간과 비례하여 높은 일차분해율이 도출되었으며, 조사시간이 2시간 이상인 실험군의 재성장 시 비성장속도 (𝜇)는 2시간 미만인 실험군 대비 비성장속도 (𝜇)가 상대적으로 낮은 것으로 확인되었다. 따라서 정체수역 내 장기적인 (30일) 조류 성장억제를 위해서는 최소한 2시간 이상의 초음파 조사가 필요한 것으로 판단되나, 조류 성장억제를 위한 적정 초음파 조사시간은 정체수역의 규모, 수심, 흐름속도, 조류 농도 등의 다양한 현장조건에 따라 결정돼야 하며, 실제 적용 가능성을 높이기 위한 추가 연구가 필요한 것으로 판단된다. 초음파의 영향으로 인한 M. aeruginosa의 세포 표면 및 내부형질 변화를 관찰한 결과, 조류 세포 표면 및 세포막의 손상이 명확히 관측되었으며, 대조군 대비 실험군의 M. aeruginosa의 기낭 파괴 및 교란이 확인되었다.

• Advances in Traditional Medicine
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• 제1권2호
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• pp.1-5
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• 2000