• Natural Product Sciences
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• v.24 no.4
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• pp.293-297
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• 2018

Sasa quelpaertensis Nakai leaves contain a mixture of polysaccharides, amino acids, and polyphenols, which mediate various biological activities. For efficient utilization of its leaf, we reported the preparation procedure for phytochemical-rich extract (PRE) using the leaf residue, which was by-product of hot water extraction. This study was undertaken to evaluate the effects of PRE and its major constituent, p-coumaric acid,on the growth of several human cancer cell lines (MKN-74, MKN-45, SNU-1, SNU-16, and HL-60). The ethyl acetate fraction of PRE and p-coumaric acid significantly inhibited the proliferation of MKN-74 and HL-60 cells, respectively, and induced cell apoptosis, down-regulated Bcl-2 and poly (ADP-ribose) polymerase levels, and up-regulated those of Bax and caspase-3. These results show the potential utility of S. quelpaertensis Nakai leaves in cancer prevention.

• Natural Product Sciences
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• v.15 no.1
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• pp.1-7
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• 2009

This study was performed to investigate the cell growth inhibitory effect of tissue cultured root of wild Panax ginseng C.A. Mayer (tcwPG). The human stomach carcinoma cell line, MKN 74, was incubated with 70% EtOH extract of tcwPG or Panax ginseng C.A. Mayer (PG) for 24 hrs. tcwPG inhibited cell growth at a concentration of $250{\mu}g/ml$. However, Panax ginseng extract did not inhibit cell growth at the same concentration. We also tested the ethyl acetate and $H_2O$ fractions of tcwPG. The inhibitory effect of the ethyl acetate fraction on cell proliferation in MKN 74 cells was more potent than that of the crude extract, and the inhibitory effect of the $H_2O$ fraction was less than that of the ethyl acetate fraction. When we separated tcwPG into polar and non-polar saponin fractions and then measured cell growth inhibition, the non-polar saponin in tcwPG exhibited cytotoxicity. To compare the effects of tcwPG on various cancer cell lines, we measured cytotoxicity in MKN 74 (stomach cancer cell line), SW 620 (colon cancer cell line) and PC 3 (prostate cancer cell line). All three cell lines showed cell growth inhibition, and the cell growth inhibitory effects were not quite different in the various cell lines. The non-polar saponins of tcwPG arrested PC 3 cells at G1-phase as did Panax ginseng.

• 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 Korean Journal of Physiology and Pharmacology
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• v.11 no.2
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• pp.65-70
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• 2007

Chinese herb medicines have traditionally been used to treat or alleviate the symptom of various diseases. The rationale for use of certain herbs to certain disorder is now getting unveiled by modern technology. In the present study, we investigated whether herb mix extract(HMX), which is alleged to be useful for gastric ulcer, protects stomach from oxidative stress. Rats were allowed to normal diet with and without HMX (1, 5, 10 mg/kg) for 30 days. To induce gastric ulcer, ethanol (75%, 1.5 ml) or acidified aspirin (100 mg/kg in 0.2 N HCl) was administered by oral route in 24 h-fasted rats and examined the gastric ulceration(bleeding) by measuring the size 1 h after the treatment. Results indicated the area of gastric bleeding was significantly less in HMX fed rats than in normal diet fed ones, and it was dependent on the duration and amount of HMX. To investigate the underlying mechanism by which HMX protects stomach from oxidative stress, expression of enzymes like heme oxygenase (HO), cyclooxygenase (COX), and inducible nitric oxide (iNOS) were investigated in MKN-74 cells, where aspirin or H. pylori was introduced. The results were compared with RAW 264.7 cells to check if there's cell specificities exist. The expression of HO-1 but not COX-2, iNOS was significantly increased by HMX. Furthermore, HO-1 inhibitor, SnPP IX reduced the HO-1 activity and reversed the survival rate in HMX-treated MKN-74 cells. There's no difference between RAW 264.7 cells and MKN-74 cells. We, thus, concluded that HMX is beneficial for protection from oxidative injury, and induction of HO-1 by HMX in gastric cells is, at least, responsible for protection from oxidative stress such as ethanol, aspirin and possibly H. pylori infection.

• 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.

• Journal of Life Science
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• v.31 no.3
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• pp.266-279
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• 2021

The present study examined the cytotoxic effects of a Smilax china L. extract (SCLE) in human cancer (A-549, MCF-7, MDA-MB-231, U87-MG, AGS, MKN-74, and SNU-601) and normal MRC-5 fibroblasts, as well as in mesenchymal stem cells derived from dental tissue (DSC). The 50% inhibitory concentration (IC50) values for SCLE were significantly (p<0.05) lower in the cancer cell lines (A-549, MCF-7, MDA-MB-231, U87-MG, AGS, MKN-74 and SNU-601) than in the MRC-5 and DSC cells. Cell growth was significantly (p<0.05) more inhibited in the cancer cell lines treated with 200 ㎍/ml SCLE than in the normal MRC-5 and DSC, and anoikis-like floating cell morphology was observed in the SCLE-treated cancer cells. The cells detached by SCLE treatment were retrieved daily and assayed for viability and telomerase activity. Cells retrieved at 4 days showed significantly decreased viability and telomerase activity (p<0.05), as well as apoptosis-like abnormal morphology, when compared to cells retrieved in the previous 3 days. The ratio of apoptosis and cells in the G1 phase was significantly (p<0.05) increased in the A-549, AGS, and MCF-7 cancer cells treated with SCLE for 4 days compared to untreated controls. However, after SCLE treatment, cell adhesion was not increased by application of an inhibitor of the associated protein kinase (ROCK) that mainly contributes to the increase in cell attachment. This suggests that the cellular detachment by SCLE is probably controlled by a Rho-independent mechanism(s). These observations indicate that SCLE readily induces anoikis in cancer cells and could serve as a potent agent for cancer chemotherapy.

• Natural Product Sciences
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• v.15 no.2
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• pp.96-100
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• 2009

A novel gastric ulcer healing formulation, a mixture of Dioscoreae Rhizoma, Halloysitum Rubrum and Ostreae Testa (Dihaos), was examined for gastric ulcer healing effects. The effect of Dihaos was assessed in various gastric ulcer models in rats. Oral administration of Dihaos significantly reduced HCl-ethanol-induced gastric ulcers. Dihaos also significantly reduced gastric and duodenal ulcers induced by cysteamine. Ostreae Testa decreased secretion of gastric juice and increased the pH of gastric juice. Furthermore, the extracts of Dioscoreae Rhizoma affected the cell proliferation of MKN 74 cells. These results suggest that the healing effect of Dihaos on gastrohemorrhagic lesions results from its protective effect against acid secretion and proliferation of mucosal cells in induced gastric ulcers in rats.

• Journal of Life Science
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• v.28 no.10
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• pp.1201-1211
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• 2018

The study compared the anti-aging, anti-adipogenesis, and anti-tumor effects of epigallocatechin-3- gallate (EGCG) in various cancer cell lines (SNU-601, MKN74, AGS, MCF-7, U87-MG, and A-549) and normal cell lines (MRC-5 fibroblasts, dental tissue-derived mesenchymal stem cells [DSC], and 3T3-L1 pro-adipocytes). Half inhibitory concentration ($IC_{50}$) values were significantly (p<0.05) higher in normal cell lines (~50 uM), when compared to that in cancer cell lines (~10 uM). For anti-aging effects, MRC-5 and DSC were exposed to 10 uM EGCG for up to five passages that did not display any growth arrest. Population doubling time and senescence-related ${\beta}-galactosidase$ ($SA-{\beta}-gal$) activity in treated cells were similar to untreated cells. For anti-adipogenic effects, mouse 3T3-L1 pre-adipocytes were induced to adipocytes in an adipogenic differentiation medium containing 10 uM EGCG, but adipogenesis in 3T3-L1 cells was not inhibited by EGCG treatment. For anti-tumor effects, the cancer cell lines were treated with 10 uM EGCG. PDT was significantly (p<0.05) increased in EGCG-treated SNU-601, AGS, MCF-7, and U87-MG cancer cell lines, except in MKN74 and A-549. The level of telomerase activity and cell migration capacity were significantly (p<0.05) reduced, while $SA-{\beta}-gal$ activity was highly up-regulated in EGCG treated-cancer cell lines, when compared to that in untreated cancer cell lines. Our results have demonstrated that EGCG treatment induces anti-tumor effects more efficiently as noted by decreased cell proliferation, cell migration, telomerase activity, and increased $SA-{\beta}-gal$ activity than inducing anti-aging and anti-adipogenesis. Therefore, EGCG at a specific concentration can be considered for a potential anti-tumor drug.

• IMMUNE NETWORK
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• v.12 no.2
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• pp.66-69
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• 2012

The immunological death induction by EY-6 on the human tumor cell lines was screened. Human colon carcinoma (HCT15, HCT116), gastric carcinoma (MKN74, SNU668), and myeloma (KMS20, KMS26, KMS34) cells were died by EY-6 treatment with dose-dependent manner. CRT expression, a typical marker for the immunological death, was increased on the EY-6-treated colorectal and gastric cancer cells. Interestingly, the effects on the myeloma cell lines were complicated showing cell line dependent differential modulation. Cytokine secretion from the EY-6 treated tumor cells were dose and cell-dependent. IFN-${\gamma}$ and IL-12 secretion was increased in the treated cells (200% to over 1000% of non-treated control), except HCT116, SNU668 and KMS26 cells which their secretion was declined by EY-6. Data suggest the potential of EY-6 as a new type of immuno-chemotherapeutics inducing tumor-specific cell death. Further studies are planned to confirm the efficacy of EY-6 including in vivo study.