• Title, Summary, Keyword: cancer cell lines

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CD44 and CD133 as Cancer Stem Cell Markers for Gastric Cancer

  • Lee, Hyun-Joo;Choi, Young-Sil;Kim, Sung-Joo;Moon, Hyoun-Jong
    • Journal of Gastric Cancer
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    • v.10 no.3
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    • pp.99-105
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    • 2010
  • Purpose: Currently, the two most influential gastric stem cell marker candidates are CD44 and CD133. The aim of this study was to make a comparison and determine the appropriate marker for use in gastric cancer stem cell research. Materials and Methods: We analyzed the expressions of CD44, CD133, and CD24 from the gastric cancer cell lines MKN45, MKN74, KATO-III, NCI-N87, SNU-1, SNU-216, SNU-601, SNU-638, and SNU-688 using flow cytometry. In addition, we measured the change in viability after applying 5 fluorouracil (5-FU) to the MKN45, MKN74, KATO-III, and NCI-N87 cell lines using a Cell Counting Kit 8. Results: CD133 expression was above moderate in the KATO-III, SNU-216, SNU-601 cell lines, whereas it was below 1% in the remaining cell lines. CD44 was expressed at levels above 5% in all gastric cancer cell lines. The effect of 5-FU on viability and CD133 or CD44 expression in the cell lines were not related. Conclusions: Expression of CD133 positive cells was insufficient in the gastric cancer cell lines. Therefore, of the cell lines tested, CD44 was the most appropriate tumor maker for research on gastric cancer stem cells.

The effects of human milk proteins on the proliferation of normal, cancer and cancer stem like cells

  • Kang, Nam Mi;Cho, Ssang-Goo;Dayem, Ahmed Abdal;Lee, Joohyun;Bae, Seong Phil;Hahn, Won-Ho;Lee, Jeong-Sang
    • Analytical Science and Technology
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    • v.31 no.6
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    • pp.232-239
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    • 2018
  • Human breast milk (HBM) provides neonates with indispensable nutrition. The present study evaluated the anti-cancer activity of diluted and pasteurized early HBM (< 6 weeks' lactation) on human breast cancer cell lines. The cell lines MCF7 and MDA-MB231 were exposed to 1 % HBM from the 1st, 3rd, and 6th weeks of lactation and exhibited reduced proliferation rates. As controls, breast cell lines (293T and MCF-10A), breast cancer cell lines (MCF-7 and MDA-MB-231), and $CD133^{hi}CXCR4^{hi}ALDH1^{hi}$ patient-derived human cancer stem-like cells (KU-CSLCs) were treated with prominent milk proteins ${\beta}$-casein, ${\kappa}$-casein, and lactoferrin at varying doses (10, 50, and $100{\mu}g$) for 24 or 48 hrs. The impact of these proteins on cell proliferation was investigated. Breast cancer cell lines treated with ${\kappa}$-casein and lactoferrin exhibited significantly reduced viability, in both a dose- and time-dependent manner. Interestingly, ${\kappa}$-casein selectively impacted only cancer (but not normal breast) cell lines, particularly the more malignant cell line. However, ${\beta}$-casein-exposed human breast cancer cell lines exhibited a significantly higher proliferation rate. Thus, ${\kappa}$-casein and lactoferrin appear to exert selective anti-cancer activities. Further studies are warranted to determine the mechanisms underlying ${\kappa}$-casein- and lactoferrin-mediated cancer cell-selective cytotoxic effects.

in vitro Assessment of Antineoplastic Effects of Deuterium Depleted Water

  • Soleyman-Jahi, Saeed;Zendehdel, Kazem;Akbarzadeh, Kambiz;Haddadi, Mahnaz;Amanpour, Saeid;Muhammadnejad, Samad
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.5
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    • pp.2179-2183
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    • 2014
  • Background: In vitro, in vivo and clinical studies have demonstrated anti-cancer effects of deuterium depleted water (DDW). The nature of this agents action, cytotoxic or cytostatic, remains to be elucidated. We here aimed to address the point by examining effects on different cell lines. Materials and Methods: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) -based cytotoxicity analysis was conducted for human breast, stomach, colon, prostate cancer and glioblastoma multiforme cell lines as well as human dermal fibroblasts. The cell lines were treated with decreasing deuterium concentrations of DDW alone, paclitaxel alone and both. One way analysis of variance (ANOVA) was used for statistical analysis. Results: Treatment with different deuterium concentrations of DDW alone did not impose any significant inhibitory effects on growth of cell lines. Paclitaxel significantly decreased the survival fractions of all cell lines. DDW augmented paclitaxel inhibitory effects on breast, prostate, stomach cancer and glioblastoma cell lines, with influence being more pronounced in breast and prostate cases. Conclusions: DDW per se does not appear to have inhibitory effects on the assessed tumor cell lines as well as normal fibroblasts. As an adjuvant, however, DDW augmented inhibitory effects of paclitaxel and thus it could be considered as an adjuvant to conventional anticancer agents in future trials.

Study of Mylabris Phalerata on Anti-cancer Effects in Some Kinds of Cancer Cells (반모가 수종의 인체 암세포에 미치는 영향)

  • Kim, Jin-Sung;Yoon, Sang-Hyub;Ryu, Bong-Ha;Ryu, Ki-Won;Jung, Myung-Chai
    • The Journal of Internal Korean Medicine
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    • v.25 no.2
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    • pp.202-213
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    • 2004
  • Object : Objective: This study was conducted to investigate the anti-cancer effects of Mylabris phalerata (반모) in some kinds of cancer cells. Materials and Methods: Some kinds of cancer cells lines were treated. We used nine kinds of cancer cell lines, such as stomach cancer cells (Kato), lung cancer cells (Calu-1, NCI-H 1395), urinary bladder cancer cells (HS789T), bone cancer cells (Saos-2), brain cancer cells (SK-N-MC), liver cancer cells (Hep-G2), skin cancer cells (Mo-1) and prostate cancer cells (PC-3) with the water decoction of Mylabris phalerata. The histological changes of all cell lines in the media (RPMI-1640) containing the decoction of Mylabris phalerata were observed and we examined cell death assay by trypan blue exclusion testing was examined. Finally, the change of mitochondrial membrane potential was measurd and the inhibitory effect of Mylabris phalerata on cell increase was examined by analyzing the cell cycle. Results: In histologic change all cancer cell lines showed withdrawn and floating appearance that is typical in cellular impairment. Most of the cell lines showed over 50% death rate after 24 hours in trypan blue exclusion tests. Especially the stomach, urinary bladder. brain and liver cell lines showed over 30% death rate after 12 hours. All cell lines treated with Mylabris phalerata were less stained than the control group and the mitochondrial membrane potential in the Mylabris phalerata treated cell lines was markedly lower than that in the control group. The measurement of DNA quantity in all cell lines showed the disappearance of the peak and the thickened left axis, which suggests that all cellular DNA degraded. Conclusion: Mylabris phalerata had cytotoxicity on various kinds of cancer cell lines and the mechanism of that was the impairment of mitochondria by the breakdown of the mitochondrial cell membrane. We propose that this is in part attributable to the destruction of DNA in cancer cells.

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Downregulation of ARFGEF1 and CAMK2B by promoter hypermethylation in breast cancer cells

  • Kim, Ju-Hee;Kim, Tae-Woo;Kim, Sun-Jung
    • BMB Reports
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    • v.44 no.8
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    • pp.523-528
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    • 2011
  • To identify novel genes that are regulated by promoter methylation, a combinational approach involving in silico mining followed by molecular assay was performed. From the expression microarray data registered in the European bioinformatics institute (EBI), genes showing downregulation in breast cancer cells were initially screened and then selected by e-Northern analysis using the Unigene database. A series of these in silico methods identified CAMK2B and ARFGEF1 as candidates, and the two genes were revealed to be hypermethylated in breast cancer cell lines and hypomethylated in normal breast cell lines. Additionally, cancer cell lines showed downregulated expression of these genes. Furthermore, treatment of the cancer cell lines with a demethylation agent, 5-Aza-2'-deoxycytidine, recovered expression of CAMK2B and ARFGEF1, implying that hypermethyaltion silenced gene activity in cancer cells. Taken together, promoter methylations of CAMK2B and ARFGEF1 are novel epigenetic markers identified in breast cancer cell lines and can be utilized for the application to clinical cancer tissues.

제 3세대 백금착체 항암제 신약개발 2. Antitumor activity and ex vivo pharmacodynamics of SKI 2053R

  • 박재갑;홍원선;방영주;조용백;태주호;김훈택;김대기;김기협;김노경
    • Proceedings of the Korean Society of Applied Pharmacology
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    • pp.74-74
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    • 1993
  • The in vitro cytotoxicity of SKI 2053R was evaluated against human tumor cell lines along with those of cisplatin and carboplatin using MTT assay. The cell lines tested were two human lung cancer cell lines and five human stomach cancer celt lines. The level of cytotoxic effects of SKI 2053R against two human lung cancer cell lines was located between cisplatin and carboplatin. However, the cytotoxic activity of SKI 2053R against five human stomach cancer cell lines was similar to that of cisplatin. SKI 2053R is considered to be selectively cytotoxic toward human stomach cancer cell lines. We carried out pharmacokinetic and ex vivo phrmacodynamic studies of SKI 2053R in beagle dogs to predict the clinical antitumor effect of SKI2053R, comparing with those of cisplatin and carboplatin. In ex vivo pharmacodynamics which used MTT assay as bioassay on the 2 lung and 5 stomach cancer cell, mean antitumor indexes (ATIs) of SKI 2053R were highest among three compounds in both lung and stomach cancer cell lines, especially in stomach cancer cell. Much higher ATI profile and maximal inhibition rates of SKI 2053R appeared in the stomach cancer cells will give desirable advantages to clinical trial s against gastric carcinoma. The anti tumor activity and target organ toxicity of SKI 2053R were compared with those of cisplatin on stomach cancer cell line, KATO III xenografted into nude BALB/c(nu/nu) mice. All groups of cisplatin and SKI 2053R showed active tumor regression. The inhibition rates(IR) of SKI 2053R were higher than that of cisplatin on the basis of mean IR. Though the loss of body weight was observed in all groups from the first week, the SKI 2053R group recovered it soon from the third week after the initiation of treatment, maintaining the most active anti tumor activity among three groups.

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ANTICANCER EFFECT OF CKD-602(BELOTECAN, CAMTOBELL$^{(R)}$) ON THE ORAL CANCER CELL LINES (구강암 세포주에 대한 CKD-602의 항암 효과)

  • Yun, Pil-Young;Ok, Yong-Ju;Myoung, Hoon;Lee, Jong-Ho;Kim, Myung-Jin
    • Journal of the Korean Association of Oral and Maxillofacial Surgeons
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    • v.31 no.1
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    • pp.7-12
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    • 2005
  • Purpose: CKD-602, a newly developed water-soluble campthotecin analogue, is a anticancer agent which act as a DNA topoisomerase I inhibitor. CKD-602 is known as more potent and tolerable agent. The main purposes of this study were to measure the cytotoxic effect of CKD-602 on the oral cancer cell lines and to evaluate the apoptotic aspect of dead cells. Materials and Methods: To determine the cytotoxic effect of CKD-602 on the oral cancer cell lines in comparison with various cell lines, such as lung cancer and colon cancer cell lines, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay was performed. And apoptosis was analyzed using fluorescence-activated cell sorting(FACS) system. Results: CKD-602 decreased the viability of malignant cells in a dose dependent manner and in a time dependent manner. CKD-602 showed excellent cytotoxicity to the oral cancer cell lines. Also, apoptotic portion was increased in a dose dependent manner. Conclusion: These findings indicated that CKD-602 induced apoptotic cell death in the various cell lines including oral cancer cell lines. From the results, it was suggested that CKD-602 would be a potential therapeutic agent for the oral cancer. More successive researches on the anticancer effect of CKD-602 should be performed.

Every Single Cell Clones from Cancer Cell Lines Growing Tumors In Vivo May Not Invalidate the Cancer Stem Cell Concept

  • Li, Fengzhi
    • Molecules and Cells
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    • v.27 no.4
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    • pp.491-492
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    • 2009
  • We present the result of our research on the tumorigenic ability of single cell clones isolated from an aggressive murine breast cancer cell line in a matched allografting mouse model. Tumor formation is basically dependent on the cell numbers injected per location. We argue that in vivo tumor formation from single cell clones, isolated in vitro from cancer cell lines, may not provide conclusive evidence to disprove the cancer stem cell (CSC) theory without additional data.

Effects of $17{\beta}$-Estradiol and Estrogen Receptor Antagonists on the Proliferation of Gastric Cancer Cell Lines

  • Kim, Myung-Jin;Cho, Sung-Il;Lee, Kun-Ok;Han, Hyung-Joon;Song, Tae-Jin;Park, Seong-Heum
    • Journal of Gastric Cancer
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    • v.13 no.3
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    • pp.172-178
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    • 2013
  • Purpose: The aims of this study were as follow: 1) to de scribe the expression status of estrogen receptor-${\alpha}$ and -${\beta}$ mRNAs in five gastric carcinoma cell lines; 2) to evaluate in vitro the effects of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of the cell lines. Materials and Methods: Detection of estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNA in five human gastric cancer cell lines (AGS, KATO III, MKN28, MKN45 and MKN74) was made by the reverse transcription-polymerase chain reaction system. To evaluate the effect of $17{\beta}$-estradiol and estrogen receptor antagonists on the proliferation of gastric cancer cell line, the cell lines which expressed both es trogen receptors were chosen and treated with $17{\beta}$-estradiol and estrogen receptor antagonists (methyl-piperidino-pyrazole and pyrazolo [1,5-a] pyrimidine). Cell proliferation was assessed with the methylthiazol tetrazolium test. Results: Estrogen receptor-${\alpha}$ and estrogen receptor-${\beta}$ mRNAs were expressed in three (KATO III, MKN28 and MKN45) and all of the five gastric cancer cell lines, respectively. At higher concentrations, $17{\beta}$-estradiol inhibited cell growth of MKN28, MKN45 and KATO III cell lines. Neither estrogen receptor-${\alpha}$ nor estrogen receptor-${\beta}$ antagonist blocked the anti-proliferative effect of $17{\beta}$-estradiol. Conclusions: Our results indicate that estrogen receptor-${\beta}$ mRNAs are preferentially expressed in gastric cancers and also imply that hormone therapy rather than estrogen receptor blockers may be a useful strategy for the treatment of estrogen receptor-${\beta}$ positive gastric cancer. Its therapeutic significance in gastric cancer are, however, limited until more evidence of the roles of estrogen receptors in the gastric cancer are accumulated.