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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cranberry extract possesses potent antioxidant capacity and antiproliferative activity against cancer in vitro and in vivo. The objectives of this study were to determine whether the cranberry extract inhibited proliferation of human gastric cancer SGC-7901 cells and human gastric tumor xenografts in the Balb/c nu/nu mouse. Cranberry extract at doses of 0, 5, 10, 20, and 40 mg/mL significantly inhibited proliferation of SGC-7901 cells, and this suppression was partly attributed to decreased PCNA expression and apoptosis induction. In a human tumor xenograft model, the time of human gastric tumor xenografts in the mouse was delayed in a dose-dependent manner. A dose-response inhibition was also observed in the averages of size, weight, and volume of tumor xenografts in the mouse between the control and cranberry-treated groups. These results demonstrate fresh cranberries to be a chemopreventive reagent.
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PMID:Cranberry phytochemical extract inhibits SGC-7901 cell growth and human tumor xenografts in Balb/c nu/nu mice. 1910 87

One obstacle of cancer therapy is the development of cancer resistance to chemotherapy. The molecular mechanisms by which the resistance is developed remain to be fully understood. Apoptosis repressor with caspase recruitment domain (ARC) is an endogenous antiapoptotic protein. Here, we report that ARC contributes to chemotherapy resistance by abolishing mitochondrial fission mediated by dynamin-related protein-1 (Drp1). Our results show that both HeLa and human gastric cancer (SGC-7901) cells have a high expression level of ARC. Doxorubicin at a low dose can slightly induce apoptosis in HeLa and SGC-7901 cells. In contrast, knockdown of ARC by its RNA interference enables the same low dose of doxorubicin to significantly induce apoptosis in HeLa and SGC-7901 cells. These data indicate that ARC is responsible for the cell resistance to doxorubicin treatment. Mitochondrial fission has recently been shown to be involved in triggering apoptosis. In exploring the molecular mechanism by which ARC participates in antagonizing doxorubicin-induced apoptosis, we observed that doxorubicin is able to induce mitochondrial fission that can be inhibited by ARC. Our results further show that Drp1 accumulates in mitochondria and mediates the signal of doxorubicin to induce mitochondrial fission. ARC is able to prevent Drp1 accumulations in mitochondria. Finally, we identified that PUMA is required for Drp1 accumulations in mitochondria. ARC inhibits Drp1 accumulations in mitochondria by directly binding to PUMA. Taken together, our results reveal a chemotherapy-resistant model in which ARC inhibits PUMA-mediated Drp1 accumulations in mitochondria and the consequent mitochondrial fission.
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PMID:Apoptosis repressor with caspase recruitment domain contributes to chemotherapy resistance by abolishing mitochondrial fission mediated by dynamin-related protein-1. 1914 62

Natural vitamin E is a mixture of two classes of compounds, tocopherols and tocotrienols. Recent research has revealed that tocotrienols, especially gamma-tocotrienol, exhibit not only the same antioxidant ability as tocopherols, but also remarkable anticancer capacity in cancer cell lines. In this study, the invasion and metastatic capacities of gastric adenocarcinoma SGC-7901 cells and the correlation with antimetastasis mechanisms induced by gamma-tocotrienol were explored. The results showed the inhibitory effects of gamma-tocotrienol at doses of 15, 30, 45 and 60 mumol/L for 48 h on cell migration and cell matrigel invasion; activities of matrix metalloproteinase (MMPs) increased in SGC-7901 cells when compared to the control group (P<.05 or P<.01). An increasing trend in the chemotactic responses to fibronectin (FN) in SGC-7901 cells was found in the gamma-tocotrienol treatments. SGC-7901 cell attachment decreased in the gamma-tocotrienol-treated groups in comparison with the control group (P<.01). The mRNA expressions of MMP-2 and MMP-9 showed that gamma-tocotrienol significantly reduced the matrigel invasion capability through down-regulation of the mRNA expressions of MMP-2 and MMP-9 (P<.01), and up-regulation of tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 in SGC-7901 cells by treatment with gamma-tocotrienol for 48 h (P<.05). gamma-Tocotrienol also significantly increased the mRNA expression of nm23-H1 in SGC-7901 cells (P<.01). These findings suggest a potential mechanism of gamma-tocotrienol-mediated antitumor metastasis activity and indicate the role of vitamin E as potential chemopreventative agents against gastric cancer.
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PMID:Inhibitory effects of gamma-tocotrienol on invasion and metastasis of human gastric adenocarcinoma SGC-7901 cells. 1919 66

To obtain water-soluble holothurian glycosides with high tumor suppressing activities from Apostichopus japonicus, macroporous resin, silica gel and gel-filtration column chromatograghy were used to purify the water-soluble holothurian glycosides, and their tumor suppressing activity and inducing apoptosis of tumor cells were examined in this study. The 70% ethanol fraction of macroporous resin column, the pSC-2 and pSC-3 fractions from silica gel column showed very strong tumor suppressing activity towards HeLa cells, A-549 lung cancer cells, SGC-7901 stomach cancer cells and Bel-7402 liver cancer cells. SC-2 and SC-3 fraction purified from Sephadex LH-20 gel-filtration column chromatography, with a purity above 99.6%, all had the properties of triterpenoid glycosides. Purified SC-2 fraction had remarkable tumor suppressing activity on HeLa cells in a dose- and time-dependent manner, and had prominent tumor suppressing activity to mouse S180 solid tumors in a dose-dependent manner. Besides, the SC-2 fraction also had remarkable ability in elevating mouse thymus index and spleen index. The purified SC-2 fraction could induce apoptosis of HeLa cells in a dose-dependent manner, and DNA fragmentation of HeLa cells occurred after treated 12 h with 10 mg x L(-1) and 50 mg x L(-1) of SC-2 fractions. From the results, it can be concluded that the purified SC-2 fraction of water-soluble holothurian glycosides has extremely strong tumor suppressing activity, and the suppression is realized by inducing tumor cells to undergo apoptosis. This study lays solid foundation for development of highly effective new natural anticancer agents from sea cucumbers.
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PMID:[Studies on the purification of water-soluble holothurian glycosides from Apostichopus japonicus and their tumor suppressing activity]. 1935 Aug 17

Two new dimeric phenanthrenes, bulbophythrins A (1) and B (2), were isolated from Bulbophyllum odoratissimum. Their structures were elucidated by HR-ESI-MS, 1D and 2DNMR spectroscopy. They were evaluated in vitro for their inhibitory ability against the growth of human leukemia cell lines K562 and HL-60, human lung adenocarcinoma A549, human hepatoma BEL-7402 and human stomach cancer SGC-7901. Both compounds showed significant cytotoxicity against the tested cell lines. Compound 1 exhibited some selectivity against HL-60 and BEL-7402 with IC(50) values of 1.27 x 10(-3) and 1.22 x 10(-3) micromol/ml respectively, whereas 2 was most active against A549 with IC(50) value of 1.18 x 10(-3) micromol/ml.
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PMID:Two new biphenanthrenes with cytotoxic activity from Bulbophyllum odoratissimum. 1944 15

Chimeric adenoviral vectors possessing fiber derived from human adenovirus subgroup B (Ad35) have been developed for their high infection efficiency in cell types which are refractory to adenovirus serotype 5 (Subgroup C). The present study constructed an E1B-deleted chimeric oncolytic adenovirus, SG235-TRAIL, which carries a human TRAIL gene expression cassette and whose fiber shaft and knob domains are from serotype Ad35. It was found that SG235-TRAIL preferentially replicated in gastric cancer cell lines, SGC-7901 and BGC-823 compared to in normal human fibroblast BJ cells. Also, when compared with a replication-deficient chimeric vector Ad5/35-TRAIL, SG235-TRAIL mediated a higher level of the transgene expression via viral replication in the cancer cells. Further, because of the more efficient cell-entry and infection, SG235-TRAIL induced stronger cell apoptosis than the Ad5 CRAD vector, ZD55-TRAIL. In addition, SG235-TRAIL in combination with the chemotherapeutic drug, taxol, produced a synergistic cytotoxic effect in cancer cells in vitro without causing significant toxicity to normal cells. In the gastric tumor xenograft mouse model, intratumoral SG235-TRAIL injection produced a significant antitumor effect 14 days after treatment. Pathological examination demonstrated TRAIL expression and associated apoptosis in majority of SG235-TRAIL-treated tumor cells. These results suggest that SG235-TRAIL is a potential novel, efficient anti-cancer agent, and in combination with taxol, it would be even more useful with considerably low toxic side effects.
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PMID:Concomitant use of Ad5/35 chimeric oncolytic adenovirus with TRAIL gene and taxol produces synergistic cytotoxicity in gastric cancer cells. 1944 45

Beta-sitosterol is an important phytosterol found in plant food. It has been shown to have antiproliferative effects on cancers of the colon, breast, and prostate, but its effect on stomach cancer cells in vitro is unknown. Proliferation, cytotoxicity, and apoptosis in SGC-7901 human stomach cancer cells were examined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, clone formation, lactate dehydrogenase (LDH) leakage assay, acridine orange (AO)/ethidium bromide (EB) double staining, 4',6-diamidine-2'-phenylindole dihydrochloride (DAPI) staining, comet assay, and Western blotting. The results showed that beta-sitosterol suppresses the proliferation and induces the cell cytotoxicity of SGC-7901 stomach cancer cells in a time- and dose-dependent manner. Cells treated with different concentrations of beta-sitosterol also showed changes typical of apoptosis: morphological changes, DNA damage, increased expression of pro-caspase-3 and bax (p < 0.05), and activation of pro-caspase-3 and suppression of bcl-2 expression (p < 0.05). This study therefore revealed that beta-sitosterol significantly inhibits the growth and induces the apoptosis of SGC-7901 human stomach cancer cells in vitro. The decrease of the bcl-2/bax ratio and DNA damage may be the critical mechanisms of apoptosis induced by beta-sitosterol in SGC-7901 human stomach cancer cells.
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PMID:Beta-sitosterol inhibits cell growth and induces apoptosis in SGC-7901 human stomach cancer cells. 1945 33

The radiosensitizing effects of luteolin were studied in the gastric cancer cell line SGC-7901. SGC-7901 cells were treated with luteolin or/and irradiation, and radiosensitizing effects were assessed by colony-forming assay with cells and nude mice. In order to study the underlying mechanism, the levels of apoptosis-related proteins, the activities of caspase-3 and -9, and the production of PGE2 were measured. The results showed that luteolin could enhance irradiation-induced colonogenic inhibition and the activities of Caspase-3 and -9. The remarkable down-regulation of Bcl-2 and release of cytochrome C were also observed. In addition, significantly reduced production of PGE(2) was observed in luteolin plus radiation treatment by ELISA, as well as decreased expression levels of VEGF and HIF-1 alpha. Finally, luteolin significantly enhances the radioresponse of human tumors transplanted into nude mice. Our results indicate that luteolin may be a promising radiosensitizer for use in the treatment of gastric cancer.
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PMID:Radiosensitization effect of luteolin on human gastric cancer SGC-7901 cells. 1958 87

Lycium barbarum polysaccharide (LBP) is extracted from the traditional Chinese herb Lycium barbarum, and has potential anticancer activity. However, the detailed mechanisms are largely unknown. The purpose of this study was to observe the anticancer effect of LBP on human gastric cancer, and its possible mechanisms. Human gastric cancer MGC-803 and SGC-7901 cells were treated with various concentrations of LBP for 1-5 days, and cell growth was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. Distribution of the cell cycle was analyzed by flow cytometry. Western blotting was used to indicate changes in the level of cyclins and cyclin-dependent kinases (CDKs). LBP treatment inhibited growth of MGC-803 and SGC-7901 cells, with cell-cycle arrest at the G0/G1 and S phase, respectively. We believe that this is the first study to show that LBP arrested different cell lines from the same types of cancer at different phases. The changes in cell-cycle-associated protein, cyclins, and CDKs were consistent with the changes in cell-cycle distribution. This study suggests that induction of cell-cycle arrest participates in the anticancer activity of LBP on gastric cancer cells.
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PMID:Growth inhibition and cell-cycle arrest of human gastric cancer cells by Lycium barbarum polysaccharide. 1966 55

BTG2 (B cell translocation gene 2) is downregulated in several human tumors and has been known as a tumor suppressor in carcinogenesis of thymus, prostate, kidney, and liver. However, little is known about the role BTG2 plays in gastric adenocarcinoma. In the present study, we intended to investigate the influence of BTG2 on the growth, proliferation, apoptosis, invasion and cell cycle of the gastric cancer cell lines SGC7901 and MKN45. BTG2 cDNA was insected into a constitutive vector pcDNA3.1 followed by transfection in gastric cancer cell line MKN45 and SGC7901 by using liposome. Then stable transfectants were selected and appraised. The apoptosis and cell cycles of these transfectants were analyzed by using flow cytometric assay. The growth and proliferation were analyzed by cell growth curves and colony-forming assay, respectively. The invasion of these clones was analyzed by using cell migration assay. MKN-BTG2 (MKN45 with stable transfection of BTG2 gene) and SGC-BTG2 (SGC7901 with stable transfection of BTG2 gene) grew slower than their control groups, respectively. The cell counts of MKN-BTG2 in the fourth, fifth, sixth and seventh days were significantly fewer than those of control groups (P < 0.05). Those of SGC-BTG2 in the fourth fifth, sixth and seventh days were significantly fewer than those of control groups too (P < 0.05). Cell cycle analysis showed that proportions of MKN-BTG2 and SGC-BTG2 cells in G0-G1 and S were different significantly with those of their control groups, respectively (P < 0.05). The apoptosis rate of MKN-BTG2 was significantly higher than those of control groups (P < 0.05). Results of colony-forming assay showed that the colon formation rates of MKN-BTG2 and SGC-BTG2 were lower than those of their control groups (P < 0.05). The results of cell migration assay showed that the cell migration rates of MKN-BTG2 and SGC-BTG2 were not significantly different with those of their control groups (P > 0.05). BTG2 can restrain the growth and proliferation of gastric cancer cells powerfully. It can reduce some malignant phenotype of these tumor cells. But it could not impact the ability of invasion of gastric cancer cells, so could not restrain the metastasis of gastric cancer. In gastric cancer, BTG2 could be thought as a tumor-inhibiting gene in some distance, so the gene could be a potential target of gene therapy.
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PMID:Impact of BTG2 expression on proliferation and invasion of gastric cancer cells in vitro. 1972 49


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