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Query: UMLS:C0699790 (colon cancer)
 28,837 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcium intake inhibits growth of colon cancer in vivo, the mechanisms of which are not fully elucidated. The objective of this study was to determine whether Ca2+ directly affects the growth of colon cancer cells in vitro and to compare the effects of Ca2+ on the growth of several gastroenteropancreatic cancer cells, including mouse colon cancer (MC-26), human colon cancer (LoVo and WIDR), human gastric cancer (AGS and SII), and human pancreatic cancer (PANC-1 and MIA) cells. All tumor cell lines tested grew in medium containing low concentration (approx 0.16 mM) of Ca2+. Higher concentrations of Ca2+ significantly inhibited the growth of all three colon cancer cell lines tested but had no significant effect on proliferation of the stomach and pancreatic cancer cell lines. Growth of AGS cells, in the presence of 0.1 or 0.5 mM EGTA (resulting in the loss of the extracellular Ca2+) was similar to that observed in the absence of EGTA, indicating that AGS cells were relatively insensitive to loss of extracellular Ca2+. In the presence of TMB-8, an inhibitor of intracellular Ca2+ release, the growth of colonic cancer cell lines was inhibited in a dose-dependent manner, indicating that a minimum basal level of intracellular Ca2+ was required for continued proliferation of colon cancer cells. The stomach cancer cell lines (AGS) was once again less sensitive to the effects of TMB-8 than were the colon cancer cells, indicating an inherent difference in Ca2+ requirements and sensitivity to Ca2+ for growth of different gastroenteropancreatic cancer cells in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential effects of Ca2+ on proliferation of stomach, colonic, and pancreatic cancer cell lines in vitro. 221 99

We have studied the ability of cyclosporin A (CsA) to inhibit the growth of human AGS gastric and HT29 colon carcinoma cells in vitro. Using continuous drug exposure in growth assays of cultured tumour cells we found that CsA produced a dose-dependent growth inhibition in gastric and colon cancer cells with a half-maximal effect at 5 microM and 6 microM CsA respectively. The growth inhibition of CsA was reversible in AGS cells, when the tumour cells were incubated in normal growth medium following CsA treatment. Trypan blue dye exclusion in AGS cells indicated a cytostatic rather than a cytotoxic effect in the concentration range used. Coincubation of CsA-treated cells with 10-400 U/ml interleukin-2 (IL-2) could not abrogate this growth inhibition, suggesting an IL-2 independent mechanism of action. Flow-cytometric analysis did not reveal a phase arrest of the gastric cancer cells within the cell cycle. We conclude from our experiments that CsA cytostatically and reversibly inhibits the growth of human gastric cancer cells in a dose-dependent manner. In contrast to its mechanism of action in lymphocytes, this direct antiproliferative effect of CsA seems not to be mediated by an IL-2-dependent pathway or a cell-cycle-phase arrest of the tumour cells.
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PMID:Growth inhibition of human gastrointestinal cancer cells by cyclosporin A. 779 92

Crude methanol extracts of red and white wines were added to diethyl ether in order to divide them into the anthocyanin fraction (insoluble in diethyl ether) and fractions containing other flavonoids and their derivatives (soluble in diethyl ether). However, the white wine did not contain anthocyanins (all of the methanol extract was soluble in diethyl ether). When HCT-15 cells, derived from human colon cancer or AGS cells, derived from human gastric cancer, were cultured with these fractions, the anthocyanin fraction from the red wine and the non-anthocyanic substances extracted from red and white wines suppressed the growth of the cells, and the suppression rate by the anthocyanin fraction was significantly higher than that of the other fractions. Thin-layer chromatographic analysis revealed mostly delphinidin in the anthocyanin fraction. The other fractions contained mostly flavonoids and their derivatives. The sugars in all fractions were mainly glucose, fucose, and fructose. Flow cytometric study suggested that the anthocyanin fraction blocked mostly S, G2, and M phase, and the non-anthocyanic flavonoids also blocked these phases, although the histographic pattern varied depending on the fractions. Methanol insoluble but water soluble fractions (mostly free sugars) of red and white wines did not show such suppressive effects.
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PMID:Anti-tumor effect of methanol extracts from red and white wines. 1085 37

Melanoidin, which belongs to the melanin group of molecules, was extracted from the polysaccharide biological response modifier PSK. Melanoidin was cultured together with HCT-15 cells derived from human colon cancer and with AGS cells derived from human gastric carcinoma. After four days of culture, cell count was compared with that of the control cells. Significant suppression was observed, that is, 50% suppression was shown at concentrations of melanoidin between 200 and 100 micrograms/ml. A histogram generated by flow cytometry showed elevation of the tetraploid peak and of that between diploid and tetraploid peaks, suggesting blockage of S phase and G2 to M phase of the cell cycle. Thus, melanoidins contained in the immunomodulator PSK revealed to have a direct tumor cell growth inhibitory effect.
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PMID:Direct tumor growth suppressive effect of melanoidin extracted from immunomodulator-PSK. 1085 84

Sangre de grado is an ethnomedicinal red tree sap obtained from Croton spp. that is used to treat gastrointestinal ulcers, cancer and to promote wound healing. To evaluate the potential role of sangre de grado (SdG) in cancer we examined its effects on human cancer cells, AGS (stomach), HT29 and T84 (colon). Viability of cells treated with SdG (10-200 microg/ml) decreased (P<0.01) in a dose dependent manner measured over a 24-h period. Cell proliferation at 48 h decreased (P<0.01) in all cells treated with SdG (>100 microg/ml). When cells in suspension were treated with SdG (100 microg/ml) cell adherence was severely compromised (>85%). Cells treated with SdG (100 microg/ml) underwent apoptosis as detected by nucleus condensation and DNA fragmentation determined by ELISA, and flow cytometry. Morphological changes as assessed by acridine orange. These effects were similar to that observed with Taxol (30 microM). A significant alteration of microtubular architecture was equally observed in both stomach and colon cancer cells exposed to SdG (100 microg/ml). The induction of apoptosis and microtubule damage in AGS, HT29 and T84 cells suggest that sangre de grado should be evaluated further as a potential source of anti-cancer agents.
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PMID:Sangre de grado Croton palanostigma induces apoptosis in human gastrointestinal cancer cells. 1200 1

Substantial evidence show a higher incidence of gastric cancer in smokers than nonsmokers and that cigarette smoking is highly associated with colon cancer. The present study was designed to examine the effect of cigarette smoke extracts on gastric and colon cancer cell proliferation, which is important for tumor growth. Two different cell lines were used. One was gastric cancer cell line AGS, and the other was colon cancer cell line HT-29. It was found that cigarette smoke extracts stimulated cell proliferation and c-myc expression in AGS cells. Furthermore, this proliferative action was partially blocked by the c-myc antisense. However, the extracts significantly inhibited HT-29 cell proliferation and suppressed c-myc expression. In conclusion, cigarette smoke extracts stimulated AGS cell proliferation, while inhibiting HT-29 proliferation, which were partially mediated by a c-myc-related pathway. The former action may play a contributory role in the carcinogenic action of cigarette smoking in the stomach.
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PMID:Differential effects of cigarette smoke extracts on cell proliferation in gastric and colon cells. 1274 85

Diphenyl difluoroketone (EF24), a molecule having structural similarity to curcumin, was reported to inhibit proliferation of a variety of cancer cells in vitro. However, the efficacy and in vivo mechanism of action of EF24 in gastrointestinal cancer cells have not been investigated. Here, we assessed the in vivo therapeutic effects of EF24 on colon cancer cells. Using hexosaminidase assay, we determined that EF24 inhibits proliferation of HCT-116 and HT-29 colon and AGS gastric adenocarcinoma cells but not of mouse embryo fibroblasts. Furthermore, the cancer cells showed increased levels of activated caspase-3 and increased Bax to Bcl-2 and Bax to Bcl-xL ratios, suggesting that the cells were undergoing apoptosis. At the same time, cell cycle analysis showed that there was an increased number of cells in the G(2)-M phase. To determine the effects of EF24 in vivo, HCT-116 colon cancer xenografts were established in nude mice and EF24 was given i.p. EF24 significantly suppressed the growth of colon cancer tumor xenografts. Immunostaining for CD31 showed that there was a lower number of microvessels in the EF24-treated animals coupled with decreased cyclooxygenase-2, interleukin-8, and vascular endothelial growth factor mRNA and protein expression. Western blot analyses also showed decreased AKT and extracellular signal-regulated kinase activation in the tumors. Taken together, these data suggest that the novel curcumin-related compound EF24 is a potent antitumor agent that induces caspase-mediated apoptosis during mitosis and has significant therapeutic potential for gastrointestinal cancers.
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PMID:Diphenyl difluoroketone: a curcumin derivative with potent in vivo anticancer activity. 1833 78

Although the biologic function of Reg IV is poorly understood, it has been reported that Reg IV is a potent activator of the epidermal growth factor receptor/Akt/AP-1 signaling pathway in colon cancer cells and closely linked with the inhibition of apoptosis. To clarify the role of Reg IV in gastric carcinogenesis and subsequent progression, we examined its expression by immunohistochemistry and in situ hybridization on tissue microarray containing gastric carcinoma, adjacent nonneoplastic mucosa, adenoma, intestinal metaplasia, or gastritis. Gastric carcinoma cell lines (MKN28, AGS, MKN45, KATO-III, and HGC-27) were studied for Reg IV expression by Western blot and reverse transcriptase-polymerase chain reaction followed by sequencing. Frozen samples of gastric carcinoma and adjacent nonneoplastic mucosa were subjected to Western blot, and patient serum, to enzyme-linked immunosorbent assay for Reg IV. Gastric carcinoma cell lines showed different levels of Reg IV mRNA and its encoding protein. The Reg IV protein expression was gradually decreased from intestinal metaplasia, adenoma, and carcinoma to gastritis (P < .05). The positive rate of its mRNA was higher in intestinal metaplasia than carcinoma or nonneoplastic mucosa (P < .05). Elevated serum Reg IV level in gastric carcinoma patients was detected in comparison with that in health individuals (P < .05). Reg IV expression was significantly correlated with the MUC-2 and MUC-5AC expression (P < .05). Among histologic subtypes of the World Health Organization, signet ring cell carcinoma more frequently expressed Reg IV than the others (P < .05), whereas it is the converse for the poorly differentiated group (P < .05). Our study indicated that Reg IV expression experienced up-regulation in gastric intestinal metaplasia and adenoma and then down-regulation with malignant transformation of gastric epithelial cells. It was suggested that Reg IV expression should be considered as a good biomarker for gastric precancerous lesions and was especially related to the histogenic pathway of signet ring cell carcinoma.
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PMID:The role of Reg IV gene and its encoding product in gastric carcinogenesis. 1974 May 14

We isolated a novel glycoprotein from the brown alga Laminaria japonica that has antiproliferative effects on HT-29 colon cancer cells. We also identified the mechanism by which this glycoprotein, named LJGP, induces apoptosis. MTS assays showed that LJGP inhibited the proliferation of several cancer cell lines (AGS, HepG2, HT-29) in a dose-dependent manner. Especially in HT-29 cells, proliferation was significantly decreased. LJGP treatment on HT-29 displayed several apoptotic features, such as DNA fragmentation, sub-G1 arrest, caspase-3 activation, and PARP degradation. Consistent with sub-G1 arrest, LJGP decreased the expression of Cdk2, cyclin E, cyclin D1, PCNA, E2F-1, and phosphorylated pRb. Furthermore, the increase of p27 expression was observed. We also determined that LJGP-induced apoptosis leads to the formation of a death-induced signaling complex of Fas, FADD, and procaspase-8. LJGP induced the reduction of mitochondrial membrane potential with activation of the Bcl-2 family of proteins and caspase-9. These findings suggest that LJGP inhibits HT-29 cell proliferation by inducing apoptosis, which may be mediated via multiple pathways, including the Fas signaling pathway, the mitochondrial pathway, and cell cycle arrest. Therefore, LJGP can be a useful treatment option for colon cancer in humans.
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PMID:A glycoprotein from Laminaria japonica induces apoptosis in HT-29 colon cancer cells. 2061 60

Protease-activated receptors (PARs) are a unique family of G-protein coupled receptors. PAR4, the most recently identified PAR member, was reported to be overexpressed during the progression of colon and prostate cancers. Though PAR4 mRNA was detected in normal stomach, the role of PAR4 in gastric cancer has not been investigated. In this study, differential expression of PAR4 was measured by real-time PCR (n=28) and tissue microarrays (n=74). We showed that PAR4 was located from basal to middle portions of normal gastric mucosa. PAR4 expression was remarkably decreased in gastric cancer tissues as compared with matched noncancerous tissues, especially in positive lymph node or low differentiation cancers. Furthermore, methylation of the PAR4 promoter in cell lines was assessed by treatment with 5-aza-2'-deoxycytidine and genomic bisulfite sequencing. AGS and N87 human gastric cancer cell lines did not express PAR4, as compared to HT-29 human colon cancer cell line with significant PAR4 expression. Treatment with 5-aza-2'-deoxycytidine restored PAR4 expression in AGS and N87 cells, which exhibited significantly more 5-methylcytosines in the PAR4 promoter compared with HT-29 cells. Our results revealed that down-regulation of PAR4 expression occurs frequently in gastric cancers and exhibits association with more aggressive gastric cancer. Interestingly, the loss of PAR4 expression in gastric cancers may result from hypermethylation of the PAR4 promoter.
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PMID:Decreased expression of protease-activated receptor 4 in human gastric cancer. 2163 66


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