• 제목/요약/키워드: cell growth inhibition

검색결과 1,652건 처리시간 0.027초

Trichosporon cutaneum의 균체생육(菌體生育) 및 Lipase 생산(生産)에 미치는 당류(糖類)의 영향 (Effect of Sugars on Cell Growth and Lipase Production by Trichosporon cutaneum)

  • 김성열
    • 농업과학연구
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    • 제4권1호
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    • pp.105-111
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    • 1977
  • 전보(前報)에 이어 Trichosporon cutaneum의 lipase 생산(生産)에 미치는 당류(糖類)의 영향을 더욱 검토(檢討)하기 위(爲)하여 몇가지 당류(糖類)를 첨가(添加)한 대두분추출액(大豆粉抽出液) 기본배지(基本培地)를 151bs에서 20분간(分間) 살균(殺菌)하였을때 일어나는 pH 및 착색도변화(着色度變化), 착색물질(着色物質)이 균체(菌體)의 생육(生育) 및 lipase 생산(生産)에 미치는 영향, 그리고 $30^{\circ}C$에서 진탕 배양(培養)하면서 배양중(培養中)의 pH 변화(變化)와 균체(菌體)의 생육(生育) 및 lipase 생산(生産)과의 관계(關係)를 검토(檢討)하여 아래와 같은 결과(結果)를 얻었다. 1. 대두분추출액(大豆粉抽出液) 기본배지(基本培地)에 각중당류(各種糖類)를 첨가(添加)하여 살균(殺菌)하였을 때 일어나는 갈변(褐變)은 xylose 첨가구(添加區)가 가장 심(甚)하고 다음이 galactose와 mannose, glucose 첨가구(添加區)의 순(順)이 었고 maltose와 sucrose 첨가구(添加區)는 당무첨가구(糖無添加區)와 별차이(別差異)가 없었다. 2. 살균후(殺菌後)에 갈변(褐變)이 심(甚)한 것일수록 pH가 낮았다. 3. 살균중(殺菌中)에 형성(形成)된 착색물질(着色物質)은 당(糖)의 종류(種類)에 비(比)하여 균체(菌體)의 생육(生育)및 lipase 생산(生産)에 미치는 영향이 작았다. 4. lipase 생산량(生産量)이 많을수록 균체(菌體)의 생산량(生産量)이이 작았다. 5. 살균중(殺菌中)의 갈변(褐變)이 가장 심(甚)한 xylose 첨가구(添加區)에서는 균체(菌體)의 증식(增殖) 및 lipase 생산저해작용(生産沮害作用)이 약천(若千) 약화(弱化)되었다. 6. 균체(菌體)의 증식(增殖)이 왕성(旺盛)할수록 배지(培地)의 pH가 낮아졌다.

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Dunaliella salina 의 광 제한 현탁 연속배양에 의한 ${\beta}$-carotene 의 생산 (Kinetics of producing ${\beta}$-carotene from Dunaliella salina by Light Limited Turbidostat Cultivation)

  • 박영식;유호금;오상집;이현용
    • 한국미생물·생명공학회지
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    • 제21권4호
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    • pp.342-347
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    • 1993
  • It was proved that the cell growth followed a photo-inhibition model in light-limited turbidostat cultivation, having 1.06 (1/h) of maximum specific growth rate and 0.00094(kcal/$cm^2$/h) and 0.063 (kcal/$cm^2$/h) as half saturation and light inhibition constants, repectively. ${\beta}$-carotene production showed a growth related porcess. And the activation energy of Dunaliella salina was roughly estimated as 12.36 (kcal/mole) in employing Arrhenius relationship. It should also point out that relatively much porduction of ${\beta}$-carotene was observed at hight light intensity with yieding 1.04 (mg-carotene/g-dry cell/day) of specific product production rate while the cell growth was decreased. The optimal conditions of producing ${\beta}$-carotene in turbiodostat cultivation were as follows: $7.5{\times}10^{-3}$(kcal/$cm^2$/h)of light intensity, 2 (mM) and 50(mM) of nitrate and sodium bicarbonate concentrations and 100(ml/h) of $CO_2$ flow rate.

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CD8-dependent Tumor Growth Inhibition by Tumor Cells Genetically Modified with 4-1BBL

  • Kim, Hong Sung
    • 대한의생명과학회지
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    • 제27권4호
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    • pp.329-333
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    • 2021
  • We previously identified that tumor cells genetically modified with a 4-1BBL co-stimulatory molecule had anticancer effects in a CT26 mouse colorectal tumor model. To identify the distinction between immune cells in a mouse tumor model treated with tumor cells genetically modified with 4-1BBL or β-gal, we examined the immune cells in CT26-WT, CT26-βgal, and CT26-4-1BBL tumor bearing mice 21 days after tumor cell administration. The CD8+ T cells population in mice treated with tumor cells genetically modified with 4-1BBL was significantly increased on day 21 compared to that of tumor cells genetically modified with β-gal in the spleen and tumor tissue. The CD4+ T cell population was not different between the two mice groups. The Foxp3+CD25high CD4 T cell population decreased on day 21 in tumor tissues, but the decrease was not significant. We also found that CD8 T cells had pivotal roles in inhibiting tumor growth by treating mice with ant-CD4 and CD8 antibodies. These results suggest that tumor cells genetically modified with 4-1BBL could inhibit tumor growth by affecting on CD8 T lymphocytes.

속수자 추출물의 HT-29 대장암세포 증식에 대한 억제효과 (Inhibitory effects of Euphorbiae lathyridis Semen extract on cell growth in HT-29 human colon cancer cells)

  • 정효원;박용기
    • 동국한의학연구소논문집
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    • 제11권
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    • pp.52-57
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    • 2008
  • Objectives. In this study, we investigate that methanol extract of Euphorbiae lathyridis Semen contributes to growth inhibitory effect on the HT-29 human colon cancer cells. Methods. Euphorbiae lathyridis Semen (ELS) was extracted with 80% methanol. HT-29 cells were treated with different concentrations of ELS extract for 24-72 hrs. Growth inhibitory effect was determined by MTT assay. Cell apoptosis was determined by surveying caspases cascades activation using Western blot. Cell cycle arrest was analyzed by flow cytometry with PI staining. Results. Exposure to ELS extract showed in inhibitory effects on HT-29 cell growth as a dose-dependent manner. Cell growth inhibition by ELS extract was related with induction of cell apoptosis with DNA fragmentation through the activation of caspases-3, caspase-9 and PARP cleavage. Conclusion. ELS extract significantly inhibited cell growth and induced cell apoptosis in HT-29 human colon cancer cells, therefore, These results suggest that ELS extract can be used as chemoprevention agent of colon cancers.

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인체폐암세포 NCI-H460 및 A549의 증식에 미치는 삼기보폐탕의 영향 비교 (Induction of Apoptosis by Samgibopae-tang in Human Non-small-cell Lung Cancer Cells)

  • 허만규;박철;최영현;감철우;박동일
    • 동의생리병리학회지
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    • 제21권4호
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    • pp.973-981
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    • 2007
  • In the present study, we investigated the antiproliferative activity of the water extract of Samgibopae-tang (SGBPT) in NCI-H460 and A549 non-small-cell lung cancer cell lines. We found that exposure of A549 cells to SGBPT resulted in the growth inhibition in a dose-dependent manner as measured by MTT assay, however SGBPT did not affect the growth of NCI-H460 cells. The antiproliferative effect by SGBPT treatment in A549 cells was associated with morphological changes such as membrane shrinking and cell rounding up. SGBPT treatment did not induce the cell cycle arrest in both cell lines, however the frequency of sub-G1 population was concentration-dependently increased by SGBPT treatment in A549 cells. SGBPT treatment partially induced the expression of tumor suppressor p53 in A549 cells and the expression of cyclin-dependent kinase inhibitor p21(WAF1/CIP1) was markedly increased in both transcriptional and translational levels in A549 cells. The up-regulation of p21 by SGBPT occurred in a similar a concentration dependent manner to that observed with the inhibition of cell viability and induction of sub-G1 population of the cell cycle. However SGBPT treatment did not affect other growth regulation-related genes such as early growth response-1 (Egr-1), nonsteroidal anti-inflammatory drug-activated gene-1 (NAG-1), inducible nitric oxide synthease (iNOS), cyclooxygenases (COXs), telomere-regulatory factors in A549 as well as NCI-H460 cells. Taken together, these findings suggested that SGBPT-induced inhibition of human lung carcinoma A549 cell growth was aoosciated with the induction of p21 and the results provided important new insights into the possible molecular mechanisms of the anti-cancer activity of SGBPT.

Fused Polypeptide with DEF Induces Apoptosis of Lung Adenocarcinoma Cells

  • Liang, Ai-Ling;Zhang, Ting-Ting;Zhou, Ning;Huang, Di-Nan;Liu, Xin-Guang;Liu, Yong-Jun;Tu, Zhi-Guang
    • Asian Pacific Journal of Cancer Prevention
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    • 제14권12호
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    • pp.7339-7344
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    • 2013
  • To analyze the effects of a new unknown peptide DEF on the growth of tumor cells, a fused polypeptide TAT-DV1-DEF was designed and synthesized. The lung adenocarcinoma cell line GLC-82 treated with TAT-DV1-DEF was analyzed with a cell counting kit 8, and the location of polypeptides in cells was observed under laser confocal microscopy. The efficiency of polypeptide transfection and changes in nuclear morphology were analyzed by flow cytometry and fluorescence microscopy, respectively. Finally, the mechanism of tumor cell growth inhibition was evaluated by Western blotting. We found that TAT-DV1-DEF could significantly inhibit the growth of the lung adenocarcinoma cell line GLC-82, but not the normal human embryonic kidney cell line HEK-293. Polypeptides were found to be mostly localized in the cytoplasm and some mitochondria. The efficiency of polypeptide transfection in the two cell types was approximately 99%. Apoptotic nuclei were observed under fluorescence microscopy upon treatment with polypeptides and DAPI staining. Western blot analyses indicated that the polypeptide inhibition of tumor cell growth was apoptosis dependent. In the present study, we demonstrated that fused polypeptides could induce apoptosis of the lung adenocarcinoma cell line GLC-82, indicating that the new unknown peptide DEF has antitumor effects.

Accelerating Effect of $TNF-{\alpha}$ on the Rhus verniciflua-induced Growth Inhibition and Apoptosis in Human Osteosarcoma Cells

  • Kim, Hyun-Duck;Kook, Sung-Ho;Kim, Beom-Tae;Kim, Jong-Ghee;Jeon, Young-Mi;Lee, Jeong-Chae
    • Natural Product Sciences
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    • 제11권1호
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    • pp.45-49
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    • 2005
  • Previously, a flavonoid fraction, which consisted mainly of protocatechuic acid, fustin, fisetin, sulfuretin, and butein, here named RCMF [${\underline{R}}hus$ verniciflua Stokes (RVS) ${\underline{c}}hloroform-{\underline{m}}ethanol\;{\underline{f}}raction$], was prepared from a crude acetone extract of RVS which is traditionally used as a food additive and as an herbal medicine. In the present study, we investigated the effects of $TNF-{\alpha}$ on RCMF-induced growth inhibition and apoptosis induction using human osteosarcoma (HOS) cells. The results from tritium uptake and MTT assays showed that $TNF-{\alpha}$ treatment itself (10 ng/ml) did not induce any cytotoxicity, but it actively accelerated RCMF-mediated cytotoxicity of HOS cells. RCMF-induced cytotoxicity and its facilitation by $TNF-{\alpha}$ was verified to be apoptotic, based on the increased DNA fragmentation and low fluorescence intensity in nuclei after propidium iodide (PI) staining of HOS cells. This speculation was further demonstrated by monitoring the Annexin V/PI double staining which could discriminate the difference between apoptotic and necrotic deaths. Collectively, our findings indicate that $TNF-{\alpha}$ accelerates RCMF-induced cytotoxicity in HOS cells.

인삼과 계피 혼합물에 의한 in vitro에서 암세포 증식억제의 상승 효과 (Synergistic Effect of Panax ginseng and Cinnamoum Blume Mixture on the Inhibition of Cancer Cell Growth in vitro)

  • 정화령;이지영;김동청;황우익
    • Journal of Ginseng Research
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    • 제23권2호
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    • pp.99-104
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    • 1999
  • 인삼과 계피 추출물의 인체 직장암 세포(HT-29), 인체 간암 세포(HepG2)및 인체 결장암 세포(HRT-18)의 증식에 미치는 영향을 in vitro에서 확인하였다. 암세포의 배양액에서 인삼 추출물 또는 계피 추출물의 효과는 농도에 비례하여 암세포의 증식을 억제하였다. 세포증식의 억제 정도는 인삼과 계피 추출물을 단독으로 첨가한 것보다 병용하여 첨가한 경우 현저한 상승 효과를 나타내어, 낮은 인삼 농도에서도 HT-29, HepG2및 HRT-18암세포의 증식을 효과적으로 억제하였으며 심지어는 사멸시켰다. 인삼과 계피의 혼합물은 세포주기 중 G1 단계에서 S단계로의 진행을 지체시킴으로써 암세포의 증식을 억제하는 것으로 나타났다.

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Saponins from Rubus parvifolius L. Induce Apoptosis in Human Chronic Myeloid Leukemia Cells through AMPK Activation and STAT3 Inhibition

  • Ge, Yu-Qing;Xu, Xiao-Feng;Yang, Bo;Chen, Zhe;Cheng, Ru-Bin
    • Asian Pacific Journal of Cancer Prevention
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    • 제15권13호
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    • pp.5455-5461
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    • 2014
  • Background: Saponins are a major active component for the traditional Chinese medicine, Rubus parvifolius L., which has shown clear antitumor activities. However, the specific effects and mechanisms of saponins of Rubus parvifolius L. (SRP) remain unclear with regard to human chronic myeloid leukemia cells. The aim of this study was to investigate inhibition of proliferation and apoptosis induction effects of SRP in K562 cells and further elucidate its regulatory mechanisms. Materials and Methods: K562 cells were treated with different concentrations of SRP and MTT assays were performed to determine cell viability. Apoptosis induction by SRP was determined with FACS and DAPI staining analysis. Western blotting was used to detect expression of apoptosis and survival related genes. Specific inhibitors were added to confirm roles of STAT3 and AMPK pathways in SRP induction of apoptosis. Results: Our results indicated that SRP exhibited obvious inhibitory effects on the growth of K562 cells, and significantly induced apoptosis. Cleavage of pro-apoptotic proteins was dramatically increased after SRP exposure. SRP treatment also increased the activities of AMPK and JNK pathways, and inhibited the phosphorylation expression level of STAT3 in K562 cells. Inhibition of the AMPK pathway blocked the activation of JNK by SRP, indicating that SRP regulated the expression of JNK dependent oon the AMPK pathway. Furthermore, inhibition of the latter significantly conferred resistance to SRP pro-apoptotic activity, suggesting involvement of the AMPK pathway in induction of apoptosis. Pretreatment with a STAT3 inhibitor also augmented SRP induced growth inhibition and cell apoptosis, further confirming roles of the STAT3 pathway after SRP treatment. Conclusions: Our results demonstrated that SRP induce cell apoptosis through AMPK activation and STAT3 inhibition in K562 cells. This suggests the possibility of further developing SRP as an alternative treatment option, or perhaps using it as adjuvant chemotherapeutic agent for chronic myeloid leukemia therapy.