• Title/Summary/Keyword: SNU.1

Search Result 608, Processing Time 0.038 seconds

Comparative Study of Autophagy in Oxaliplatin-Sensitive and Resistant SNU-C5 Colon Cancer Cells

  • Boo, Sun-Jin;Piao, Mei Jing;Kang, Kyoung Ah;Zhen, Ao Xuan;Fernando, Pincha Devage Sameera Madushan;Herath, Herath Mudiyanselage Udari Lakmini;Lee, Seung Joo;Song, Seung Eun;Hyun, Jin Won
    • Biomolecules & Therapeutics
    • /
    • v.30 no.5
    • /
    • pp.447-454
    • /
    • 2022
  • Few studies have evaluated the role of autophagy in the development of oxaliplatin (OXT) resistance in colon cancer cells. In this study, we compared the role of autophagy between SNU-C5 colon cancer cells and OXT-resistant SNU-C5 (SNU-C5/OXTR) cells. At the same concentration of OXT, the cytotoxicity of OXT or apoptosis was significantly reduced in SNU-C5/OXTR cells compared with that in SNU-C5 cells. Compared with SNU-C5 cells, SNU-C5/OXTR cells exhibited low levels of autophagy. The expression level of important autophagy proteins, such as autophagy-related protein 5 (Atg5), beclin-1, Atg7, microtubule-associated proteins 1A/1B light chain 3B I (LC3-I), and LC3-II, was significantly lower in SNU-C5/OXTR cells than that in SNU-C5 cells. The expression level of the autophagy-essential protein p62 was also lower in SNU-C5/OXTR cells than in SNU-C5 cells. In SNU-C5/OXTR cells, the production of intracellular reactive oxygen species (ROS) was significantly higher than that in SNU-C5 cells, and treatment with the ROS scavenger N-acetylcysteine restored the reduced autophagy levels. Furthermore, the expression of antioxidant-related nuclear factor erythroid 2-related factor 2 transcription factor, heme oxygenase-1, and Cu/Zn superoxide dismutase were also significantly increased in SNU-C5/OXTR cells. These findings suggest that autophagy is significantly reduced in SNU-C5/OXTR cells compared with SNU-C5 cells, which may be related to the production of ROS in OXT-resistant cells.

Characteristics of [$^{18}F$]fluorodeoxyglucose Uptake in Human Colon Cancer Cells (사람 대장암 세포주의 [$^{18}F$fluorodeoxyglucose 섭취의 특징)

  • Kim, Chae-Kyun;Jeong, Jae-Min;Lee, Myung-Chul;Koh, Chang-Soon;Chung, June-Key
    • The Korean Journal of Nuclear Medicine
    • /
    • v.31 no.3
    • /
    • pp.381-387
    • /
    • 1997
  • Cancer tissues are characterized by increased glucose uptake. $^{18}F$-fluorodeoxyglucose(FDG), a glucose analogue is used for the diagnosis of cancer in PET studies. This study was aimed to compare the glucose uptake and glucose transporter 1(GLUT1) expression in various human colon cancer cells. We measured FDG uptake by cell retention study and expression of GLUT1 using Western blotting. Human colon cancer cells, SNU-C2A, SNU-C4 and SNU-C5, were used. The cells were incubated with $1{\mu}Ci/ml$ of FDG in HEPES-buffered saline for one hour. The FDG uptake of SNU-C2A, SNU-C4 and SNU-C5 were $16.8{\pm}1.36,\;12.3{\pm}5.55$ and $61.0{\pm}2.17cpm/{\mu}g$ of protein, respectively. Dose-response and time-course studies represent that FDG uptake of cancer cells were dose dependent and time dependent. The rate of FDG uptake of SNU-C2A, SNU-C4 and SNU-C5 were $0.29{\pm}0.03,\;0.21{\pm}0.09$ and $1.07{\pm}0.07cpm/min/{\mu}g$ of protein, respectively. Western blot analysis showed that the GLUT1 expression of SNU-C5 was significantly higher than those of SNU-C2A and SNU-C4. These results represent that FDG uptake into human colon cancer cells are different from each other. In addition, FDG uptake and expression of GLUT1 are closely related in human colon cancer cells.

  • PDF

Study for Metabolism of Resistant Production in Anticancer drug Resistant Stomach Cancer Cell SNU-1 (항암제 내성 위암 세포주 SNU-1의 내성생성기전에 관한 연구)

  • Kim, Jung-Hye;Kang, Mi-Wha;Kim, Jae-Ryong
    • Journal of Yeungnam Medical Science
    • /
    • v.6 no.2
    • /
    • pp.195-205
    • /
    • 1989
  • Development of drug resistance in tumors during treatment is a major factor limiting the clinical use of anticancer agents. When tumor cells acquire resistance to anticancer drug, they show cross-resistance to other antitumor agents. In the present study, SNU-1 cell was induced adriamycin $10^{-7}M$ drug resistance, SNU-1/ADR, in vitro culture system. We got the doubling time and number for viability test during 96 hours by MTT assay. To investigate the cross resistance of various anticancer drugs in human stomach cancer cell SNU-1 and SNU-1/ADR. We compared $IC_{50}$ (drug concentration of 50% reduction) and the relative resistance(RR). SNU-1/ADR was expressed multidrug resistant with vinblastine(RR ; 31.62), vincristine(RR ; 29.50), dactinomycin(RR ; 21.37), epirubicin(RR ; 17.78), daunorubicin(RR ; 14.12), adriamycin(RR ; 7.76), and etoposide(RR ; 4.46), and other drugs, 5-fluorouracil, cisplatin, cyclophosphamide, methotrexate, and aclarubicin, have not cross resistant with adriamycin. There was double minute chromosome in SNU-1/ADR by karyotyping although this change was not seen in SNU-1.

  • PDF

Enhanced proliferation of SNU-407 human colon cancer cells by muscarinic acetylcholine receptors

  • Park, Yang-Seo;Cho, Nam-Jeong
    • BMB Reports
    • /
    • v.41 no.11
    • /
    • pp.803-807
    • /
    • 2008
  • We investigated the expression of muscarinic acetylcholine receptors (mAChRs) and their possible involvement in the regulation of cell proliferation in four colon cancer cell lines (SNU-61, SNU-81, SNU-407, and SNU-1033) derived from Korean colon carcinoma patients. A ligand binding assay showed that all four cell lines expressed mAChRs. Treatment of the four cell lines with the cholinergic agonist carbachol led to the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2). In SNU-407 cells, carbachol significantly stimulated cell proliferation, which could be abolished by the muscarinic antagonist atropine and the ERK1/2 kinase inhibitor PD98059. These results indicate that mAChRs specifically mediate the proliferation of SNU-407 colon cancer cells via the ERK1/2 pathway.

Study on Anti-Cancer Effects of Rhus Verniciflua Stokes Extracted with Sterile Distilled Water on Two Cholangiocarcinoma Cell Lines, SNU-1079 and SNU-1196 (칠피(漆皮) 추출물의 담도암 세포주 SNU-1079와 SNU-1196에 대한 항암효과)

  • Joung, Bo-bae;Kim, Young-chul
    • The Journal of Internal Korean Medicine
    • /
    • v.36 no.1
    • /
    • pp.1-12
    • /
    • 2015
  • Objectives : This study was performed to investigate the anti-cancer effects of Rhus verniciflua Stokes (RVS) extracted with sterile distilled water on cholangiocarcinoma cell lines. Materials and Methods : Two cholangiocarcinoma cell lines, SNU-1079 and SNU-1196, were used in this study. Cells were treated with different concentrations of RVS for 24, 48, and 72 hours. Cell count, viability, apoptosis, and mRNA expression of Bax, Bcl-2, Mcl-1, survivin, caspase-3, and cyclin D1 and P21 were determined with an automatic cell counter (ADAM-MC), MTT assay, apoptosis assay (Annexin-V/PI staining), and RT-PCR. Results : All cells treated with RVS showed decreased cell counts in a dose-dependent manner. RVS inhibited proliferation of SNU-1196 in a dose-dependent manner, but SNU-1079 proliferation was inhibited in the long-time culture group in a dose-dependent manner. The proportion of early and late-stage apoptotic cells was increased by RVS in a dose-dependent manner in SNU-1196. In contrast, it was increased significantly in SNU-1079 treated with high-dose RVS. After treatment with RVS, the mRNA expression of Bcl-2 was decreased while Bax was increased in SNU-1079. Cyclin D1 mRNA levels were decreased in SNU-1196 in a dose-dependent manner. P21 expression was increased in all cells after the treatment with RVS. Conclusions : RVS appears to have potential as a therapeutic agent for cholangiocarcinoma.

Dark fermentation for hydrogen production with a new bacterium Enterobacter asburiae SNU-1 (새로운 Enterobacter asburiae SNU-1의 혐기발효에 의한 생물학적 수소생산)

  • 신종환;김미선;심상준;박태현
    • 한국전기화학회:학술대회논문집
    • /
    • 2005.07a
    • /
    • pp.177-186
    • /
    • 2005
  • 미래의 친환경 에너지인 수소에너지 생산을 위해서 생물학적인 수소생산방법에 관한 관심이 증폭되고 있다. 생물학적인 수소생산 방법에는 여러 가지가 있으나 그중 유기물을 혐기발효하여 수소를 생산하는 방법에 관한 연구가 수행되었다. 본 연구에서 혐기성 미생물인 Enterobacter asburiae SNU-1이 쓰레기 매립지 토양에서 분리되어 수소생산 조건의 최적화 실험을 수행하였다. 본 실험에 이용된 미생물의 경우는 기존에 연구 된 적이 없는 새로운 종으로써 다른 미생물과는 다른 특징을 나타내며 수소생산 능력도 뛰어난 것을 알 수 있었다. 미생물을 이용한 수소생산에 영향을 미치는 인자로는 pH, initial glucose concentration 등이 있으며 각각의 조건에서 수소생산량을 비교하였다. 실험 결과 strain SNU-1의 최적 pH는 7이었으며 최적 initial glucose concentration은 25 g/1이다 이와 같은 최적 조건에서 strain SNU-1은 6.87 mmol/l/hr의 productivity를 나타내었다. 또한 다른 미생물과 달리 미생물이 더 이상 자라지 않는 정지기에서 더 많은 수소생산량을 나타내는 특이한 거동을 보이는 것이 관찰되었다.

  • PDF

Antineoplastic Effect of Several Herbal Medicine Mixtures on SNU-80 Anaplastic Thyroid Carcinoma Cell Line (수종 한약 복합물의 역형성갑상선암세포 SNU-80에 대한 항암효과)

  • Yeo, Hyun-Soo;Lee, Min-Hye;Choi, You-Kyung;Jun, Chan-Young;Park, Jong-Hyeong
    • The Journal of Internal Korean Medicine
    • /
    • v.35 no.4
    • /
    • pp.416-427
    • /
    • 2014
  • Objectives: The purpose of this study was to investigate the antineoplastic effect of several herbal medicine mixtures (compositions of Astragalus membranaceu, Angelica gigas, Trichosanthes kirilowii, Panax ginseng, Rhus verniciflua Stokes) on the SNU-80 anaplastic thyroid carcinoma cell line. Methods: MTT assay was used to examine whether our herbal medicine mixtures decreased cell growth rate of SNU-80. Wound healing assay and Transwell invasion assay was performed to investigate whether our herbal medicine mixtures affect the migration and invasion of anaplastic cancer cells, SNU-80. ELISA assay was performed to know if our herbal medicine mixtures suppressed the expression of pro-invasive molecules, such as vascular endothelial growth factor (VEGF) and matrix metalloproteinase-2 (MMP-2) secreted from SNU-80. Results: MTT assay demonstrated that A. membranaceus:A. gigas:T. kirilowii=1:1:1 or 3:1:1, A. membranaceus:A. gigas :T. kirilowii:P. ginseng=1:1:1:1 or 3:1:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng:R. verniciflua Stokes=1:1:1:1:1 or 3:1:1:1:1 strongly suppressed the growth of SNU-80. Wound healing assay demonstrated that A. membranaceus:A. gigas=3:1, A. membranaceus:A. gigas:T. kirilowii=1:1:1 or 3:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng=1:1:1:1 or 3:1:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng:R. verniciflua Stokes=1:1:1:1:1 or 3:1:1:1:1 inhibited the migration of SNU-80. Transwell invasion assay demonstrated that A. membranaceus:A. gigas=1:1, A. membranaceus:A. gigas:T. kirilowii =1:1:1 or 3:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng=1:1:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng :R. verniciflua Stokes=1:1:1:1:1 or 3:1:1:1:1 inhibited the invasion of SNU-80. ELISA assay demonstrated that A. membranaceus :A. gigas:T. kirilowii=1:1:1 or 3:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng:R. verniciflua Stokes=1:1:1:1:1 suppressed the expression of VEGF. Also, A. membranaceus:A. gigas=1:1, A. membranaceus:A. gigas:T. kirilowii=1:1:1 or 3:1:1, A. membranaceus :A. gigas:T. kirilowii:P. ginseng=1:1:1:1 or 3:1:1:1, A. membranaceus:A. gigas:T. kirilowii:P. ginseng:R. verniciflua Stokes =1:1:1:1:1 or 3:1:1:1:1 suppressed the expression of MMP-2. Conclusions: The results obtained in this study suggest that several herbal medicine mixtures suppresse the growth and inhibit the migration and invasion of SNU-80, which is anaplastic thyroid cancer cells. Especially, A. membranaceus:A. gigas: T. kirilowii=1:1:1 mixture had a stronger anti-cancer effect.

A Comparative Study of the Anti-cancer Effects of Smilacis Chinae Rhizoma and Smilacis Glabrae Rhizoma on Stomach Cancer SNU-1 Cells (토복령(土茯苓)의 기원식물별 위암 세포 SNU-1에 대한 항암효과 비교연구)

  • Ahn, Han-Kyu;Han, Hyo-Sang;Lee, Young-Jong
    • The Korea Journal of Herbology
    • /
    • v.25 no.1
    • /
    • pp.23-31
    • /
    • 2010
  • Objectives : The purpose of this study was to compare the anticancer effects of Smilacis Chinae Rhizoma (SCR) and Smilacis Glabrae Rhizoma (SGR) on stomach cancer SNU-1 cells. Methods : The cell proliferation, apoptosis and cytokine level from the extracts were examined in order to compare the anticancer effects of SCR and SGR on SNU-1 cells. Results : SCR had greater anticancer effects than SGR in terms of the inhibition of cell proliferation and apoptosis in the SNU-1 cells. SCR decreased TGF-$\beta$ and SGR increased IL-2 in SNU-1 cells. SCR decreased more TGF-$\beta$ and increased more TNF-$\alpha$ compared to SGR. Conclusions : There were few significant differences according to the concentration and fraction, but a greater anticancer effect of SCR was shown as compared with SGR.

Multidrug Resistance and Cytotoxicity of Anticancer Drug by Verapamil in Cisplatin Resistant Human Stomach Cancer Cell (Cispatin 내성인 사람 위암 세포주 SNU-1의 복합약제내성 및 Verapamil의 효과)

  • Son, Seong-Kweon;Kim, Jung-Hye
    • Journal of Yeungnam Medical Science
    • /
    • v.9 no.1
    • /
    • pp.75-89
    • /
    • 1992
  • The development of multi drug-resistant tumor cell population is a major problem in the chemotherapy of human cancer. These cells are often cross resistant to unrelated drugs and the precise mechanisms of multidrug resistant phenotype of tumor cells has not been fully elucidated. Cisplatin resistant tumor cell(SNU-1/$Cis_5$) was induced from human stomach cancer cell line(SNU-1) in vitro. Growth profiles of survival cells were observed during 5 days by thiazolyl blue (MTT) assay. To investigate the cross resistance of various anticancer drugs in SNU-1 and SNU-1/$Cis_5$, We compared the value of $IC_{50}$ - drug concentration at 50% survival of control and gained relative resistances (RR). The RR for SNU-1/$Cis_5$ were as follows; vinblastine, > 43.0 ; epirubicin, 22.9 ; dactinomycin, 16.0 ; etoposide, 15.0 ; vincristine, 9.2 ; adriamycin, 5.7 ; aclarubicin, 5.3. But 5-fluorouracil, methotrexate, daunorubicin have not cross resistance with cisplatin. Resistant inhibition values of $10{\mu}M$ verapamil for SNU-1/$Cis_5$ were as follows; vincristine, 13.1 ; epirubicin, 10.0 ; etoposide, 6.3 ; vinblastine, 4.4 ; dactinomycin, 3.6 ; daunorubicin, 2.4. Membrane proteins of 51,400 and 81,300 daltons were identified by radioiodination with SDS-PAGE, which might represented the drug resistance.

  • PDF