Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.4.99.7 (sialyltransferase)
1,534 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

alpha-Neup5Ac-(2----3)-beta-D-Galp-(1----3)-D-GlcpNAc (2) and, alpha-Neup5Ac-(2----3)-beta-D-Galp-(1----3)-beta-D-GlcpNAcOMBn+ ++ were prepared on a large scale by the action of beta-D-Galp-(1----3)-D-GalpNAc (2----3)-alpha-sialyltransferase (partially purified from porcine liver) on beta-D-Galp-(1----3)-D-GlcpNAc and beta-D-Galp-(1----3)-beta-D-GlcpNAcOMBn, respectively. The trisaccharide 2 is the epitope of the tumor-associated carbohydrate antigen CA 50, highly expressed in human pancreatic adenocarcinoma.
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PMID:The use of porcine liver (2----3)-alpha-sialyltransferase in the large-scale synthesis of alpha-Neup5Ac-(2----3)-beta-D-Galp-(1----3)-D-GlcpNAc, the epitope of the tumor-associated carbohydrate antigen CA 50. 138 Dec 78

The expression of antigens of the blood group Lewis a/b family were studied in a series of 42 prostatectomy specimens from patients with adenocarcinoma clinically confined to the prostate; 19 of these were later reclassified as pathologic Stage C. Staining of normal or hyperplastic versus neoplastic epithelium was assessed in routinely processed, paraffin-embedded tissue using murine monoclonal antibodies and an avidin-biotin immunoperoxidase technique. Antigens screened and the antibodies used to recognize them were Lewis a (CF4C4), Lewis b and Type 1 H (NS10), monosialosyl Lewis a I (19.9), and disialosyl Lewis a and monosialosyl Lewis a II (FH7). FH7 strongly stained the benign epithelium of all 39 Lewis positive cases, suggesting that the sialyltransferase responsible for synthesis of FH7-reactive determinants is highly active in benign prostatic tissue. When compared to the reactivity of benign epithelium in Lewis positive cases, the staining of the carcinomas was markedly reduced in 18 cases (46%) and absent in 16 cases (41%). This reduction or loss of staining of the malignant epithelium was observed for all antibodies that stained the corresponding benign epithelium of each case. In only five of the cases (13%) was the intensity of staining in the carcinoma equal to that of the surrounding benign epithelium. No cases in this latter group had recurrence of disease, whereas in the other staining groups 25-33% of the cases had recurrences; median follow-up for the entire group was 78 months. No correlation was apparent between Gleason score and the staining pattern with these antigens. In summary, antigens of the Lewis a/b family are deleted in a high percentage of cases of prostatic adenocarcinoma.
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PMID:Deletion of antigens of the Lewis a/b blood group family in human prostatic carcinoma. 245 82

As described previously (I. Kijima-Suda et al., Cancer Res., 46: 858-862, 1986), a sialyltransferase inhibitor, 5-fluoro-2',3'-isopropylidene-5'-O-(4-N-acetyl-2,4-dideoxy-3,6,7,8-tetra -O- acetyl-1-methoxycarbonyl-D-glycero-alpha-D-galactooctapyranosyl)ur idine (KI-8110), inhibits pulmonary metastasis of murine colon adenocarcinoma 26 sublines of high (NL-17) and low (NL-44) metastatic potential. To investigate the mechanism of this inhibition, the effect of KI-8110 on the metastatic cascade, especially on the interaction between tumor cells and platelets which may play a crucial role in tumor cell metastasis, was examined. NL-17 cells induced irreversible platelet aggregation in heparinized human platelet-rich plasma in vitro. This activity was reduced by pretreatment of the tumor cells with KI-8110. Inhibition of aggregation was also induced by the treatment of tumor cells with neuraminidase or Limax flavus agglutinin, a lectin specific for sialic acid. Sialic acid, fucose, sialyllactose, and bovine submaxillary mucin inhibited this tumor cell-induced platelet aggregation, while galactose, mannose, lactose, alpha 1-acid glycoprotein, fetuin, and asialo-bovine submaxillary mucin did not. KI-8110 also inhibited platelet-derived growth factor-dependent growth of NL-17 cells, but showed no effect on insulin or epidermal growth factor-dependent growth of the tumor cells. Platelet-derived growth factor-induced phosphorylation of membrane protein was reduced by treatment of NL-17 cells with KI-8110. The same result was obtained in the neuraminidase-treated membrane fraction of NL-17 cells. These results suggest that KI-8110 inhibits experimental tumor cell metastasis by inhibiting the interaction between tumor cells and host platelets in at least two pathways, and this may be due to a reduction of sialic acid contents of the membrane surface of tumor cells.
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PMID:Possible mechanism of inhibition of experimental pulmonary metastasis of mouse colon adenocarcinoma 26 sublines by a sialic acid: nucleoside conjugate. 328 33

The total and sialidase-releasable sialic acid contents of murine colon adenocarcinoma 26 sublines of high (NL-17) and low (NL-44) metastatic potential were found to be positively correlated with their ability to undergo metastasis. Furthermore, sialyltransferase activity of intact NL-17 cells was higher than that of NL-44 cells. These findings suggest that sialic acid on the cell surface may play a role in the metastasis of these cells. Therefore, the effect of a sialyltransferase inhibitor, 5-fluoro-2',3'-isopropylidene-5'-O-(4-N-acetyl-2,4-dideoxy-3,6,7,8-tetra -O -acetyl-1-methoxycarbonyl-D-glycero-alpha-D-galactooctapyranosyl)u ridine (Kl-8110), on the experimental lung metastasis of NL-17 or NL-44 cells was examined. Kl-8110 inhibited the transfer of sialic acid to its endogenous acceptor in NL-17 and NL-44 cells. NL-17 or NL-44 cells were injected into the tail veins of mice, and the metastasis-inhibiting activity of Kl-8110 was evaluated on the basis of both the lung weight and the number of pulmonary surface nodules about 3 wk after the tumor cell injection and of the survival ratio of mice inoculated with the tumor cells. Pretreatment of tumor cells with Kl-8110 together with i.v. injection of Kl-8110 caused significant inhibition of pulmonary metastasis of both NL-17 and NL-44 cells. Inhibition of metastasis and prolongation of survival were also observed on i.v. injection of Kl-8110 without pretreatment of the tumor cells with Kl-8110, but the degree of inhibition was lower than that in the case of the two treatments together. Kl-8110 itself had neither cytostatic nor cytotoxic effects on NL-17 and NL-44 but reduced the retention of tumor cells in the lungs. This antimetastatic effect of Kl-8110 may be due to modification of the tumor cell surface resulting from inhibition of sialyltransferase by Kl-8110. In addition, a beta-linked sialic acid:nucleoside conjugate (Kl-8111) and an equimolar mixture of Kl-8110 and Kl-8111 (Kl-414) also inhibited the metastatic ability of NL cells to the same extent as Kl-8110 did.
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PMID:Inhibition of experimental pulmonary metastasis of mouse colon adenocarcinoma 26 sublines by a sialic acid:nucleoside conjugate having sialyltransferase inhibiting activity. 375 83

Membrane glycopeptides were examined in human colonic adenocarcinoma and normal colonic mucosa. The carbohydrates of membrane glycopeptides were found to be markedly reduced in tumor tissue and the relative proportions of the various sugars were altered. Although all of the sugars were lower in tumor tissue when compared to the adjacent normal mucosa, galactosamine, fucose, and sialic acid were more significantly reduced. Examination of the blood group activity and lectin-binding properties of membrane glycopeptides revealed that specific carbohydrate structures had changed in the tumor tissue. Most striking of these changes was the disappearance of glycoprotein-associated blood group A activity. Assay of the enzyme responsible for synthesis of the blood group A determinant showed that this glycosyltransferase activity was greatly diminished in tumor tissue. A galactosyltransferase and a fucosyltransferase were also significantly lower in the tumor tissue whereas the levels of another galactosyltransferase and a sialyltransferase were unaltered. Glycosidase activities in the normal and tumor tissues were similar. The results show that an alteration in glycoprotein biosynthesis occurred during tumorigenesis that resulted in a modified membrane glycoprotein composition and that these changes are probably a reflection of reduced levels of the enzymes responsible for glycoprotein synthesis.
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PMID:Alterations of membrane glycopeptides in human colonic adenocarcinoma. 414 May 12

Serum sialyltransferases and fucosyltransferases measured by an affinity adsorbent technique were studied in 27 exactly defined patients with malignant pulmonary diseases. Fourteen patients with benign pulmonary diseases and 56 with benign surgical diseases were used as controls. Enzyme activities were expressed as amounts of labeled precursor molecules incorporated into endogenous acceptors in counts per minute (cpm). The mean sialyltransferase activity was 583 cpm in bronchial carcinoma, 485 cpm in benign pulmonary disease and 428 cpm in benign surgical disease. The only statistically significant difference was between bronchial carcinoma and benign surgical disease. The mean fucosyltransferase activity was 813 cpm in bronchial carcinoma, 436 cpm in benign pulmonary disease and 255 cpm in benign surgical disease. All the differences were statistically significant. There were no statistically significant differences between the WHO histologic bronchial carcinoma groups. The correlation between sialyltransferase and fucosyltransferase activity in bronchial carcinoma was statistically significant (r = 0.59). In squamous cell carcinoma (N = 6), it was strongly significant (r = 0.96) and there was a significant correlation also in small cell carcinoma (N = 10; r = 0.79) but not in adenocarcinoma (N = 9; r = 0.30) and benign pulmonary disease (N = 14; r = 0.44). It is suggested that serum sialyltransferases and fucosyl transferases would not be decisive for diagnosis when used alone in bronchial carcinoma, but could be included in a screening test battery.
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PMID:Serum sialyltransferase and fucosyltransferase activities in patients with bronchial carcinoma. 631

The MAT-B1 and MAT-C1 ascites sublines of the 13762 rat mammary adenocarcinoma differ in morphology, agglutinability with concanavalin A, and xenotransplantability. Both cell lines contain a major mucin-type glycoprotein, but the MAT-C1 (xenotransplantable) subline contains a 3-fold-greater content of sialic acid on the glycoprotein than does the MAT-B1 (nonxenotransplantable) subline. The present work indicates that whole cells of both lines incorporate radioactivity from labeled CMP-sialic acid into a component which comigrates with the major glycoprotein by sodium dodecyl sulfate polyacrylamide gel electrophoresis, and that label incorporated by MAT-B1 cells is released by alkaline-borohydride treatment. Sialyltransferase can be purified from 250- to 400-fold by chromatography of a Triton X-100 extract of microsomes on CDP-agarose. The purified fraction of both cell lines has a Km for CMP-sialic acid of 0.40 +/- 0.10 mM with asialofetuin as the acceptor, and gives 35 to 40% of the activity with the acceptor asialotransferrin as with asialofetuin. When assayed with a variety of acceptors, the MAT-C1 extract showed higher sialyltransferase activity at a pH below 6.5 than did the MAT-B1 extract. Analysis of the products following incubation with lactose yields only 3'-sialyllactose for both cell lines. The results indicate that the differences in MAT-B1 and MAT-C1 sialyltransferase when assayed with glycoprotein acceptors are not large enough to account for the differences in sialic acid content of the two cell lines.
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PMID:Sialyltransferase of the 13762 rat mammary ascites tumor cells. 669 99

Total plasma sialyltransferase (ST) activity was elevated in patients with colonic adenocarcinoma; the incidence of abnormal values ranged from 33% in patients with no evidence of metastases (T2N0M0) to 86% in patients with advanced metastatic disease (T2-5N1M1). Isoenzyme analysis revealed that normal serum contains a major band (ST2) probably derived from red cells, and a minor band (ST1) thought to be derived from platelets. An additional band, designated STN, intermediate in mobility between the two other bands, was found in patients with colonic adenocarcinoma, ranging in incidence from 50% to 86% in patients free of metastases and those with widespread metastases. Histological studies suggested that this abnormal isoenzyme was more likely to occur in the serum of patients whose tumor was well differentiated.
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PMID:Plasma sialyl transferase total and isoenzyme activity in the diagnosis of cancer of the colon. 706 76

Sodium butyrate and dimethylsulfoxide (DMSO) have marked effects on the growth, morphology, and biochemistry of two human colonic adenocarcinoma cell lines in culture. Doubling times were increased between 18% and 660% while cell viability was unaffected. Both cell lines formed colonies in soft agar in the absence of butyrate of DMSO, but no colonies were observed in the presence of these agents. However, no differences in in vivo tumorigenicities, when cells were implanted in athymic mice, were seen following treatment. Gross morphological alterations including cell enlargement, process formation, and cellular flattening occurred during culture in butyrate or DMSO. Acrylamide gel electrophoresis in sodium dodecyl sulfate revealed no change in membrane protein constituents, but autoradiographic analysis of membrane glycoproteins demonstrated differences between treated and untreated cells. Ganglioside compositions were altered, and a sialyltransferase required for the synthesis of GM3 ganglioside was elevated by butyrate. Although cytoplasmic aminooligopeptidase remained unaffected by butyrate or DMSO, brush border-associated activity was enhanced by butyrate. Alkaline phosphatase also rose dramiatically during culture in butyrate but was not enhanced by DMSO.
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PMID:Effects of sodium butyrate and dimethylsulfoxide on biochemical properties of human colon cancer cells. 735 11

A human colonic adenoma cell line PC/AA derived from a familial polyposis coli patient was passaged in culture to form an intermediate premalignant clonogenic variant AA/C1 and, upon treatment with differentiating and carcinogenic agents, a cell line AA/C1/SB10 which is tumourigenic in nude mice. These three mucin-secreting cell lines have been used as a model to study the changes in O-glycan biosynthesis during the progression to cancer. Several glycosyltransferases involved in the synthesis, elongation and termination of the common O-glycan core structures were found to decrease in the progression sequence towards adenocarcinoma. Higher activity of a number of enzymes was seen in the intermediate cell line. O-glycan biosynthesis in the original PC/AA cell line was closest to the normal human colonic phenotype, since all four common mucin O-glycan cores and their extended structures could be synthesized; core 3 beta 3-GlcNAc-transferase and alpha 6-sialytransferase acting on GalNAc-mucin were still detectable and core 2 beta 6-GlcNAc-transferase activity was accompanied by core 4 and I beta 6-GlcNAc-transferase activities. During progression towards adenocarcinoma, the expression of alpha 6-sialyltransferase, core 3 beta 3-GlcNAc-transferase, core 4 and I beta 6-GlcNAc-transferases were turned off. Using monoclonal antibodies, Tn antigen, sialyl-Tn antigen, O-acetyl-sialomucin and sialyl-Lea determinants were not detected in secreted or cellular mucin isolated from any of the cell lines. The exposure of MUC1 epitopes was seen in the malignant line, whereas sialyl-Lex determinants were found only in the premalignant PC/AA line. Sulfotransferase activities using core 1 substrate, Gal beta 1-3GalNAc alpha-benzyl, were high in PC/AA cells and progressively decreased upon development to adenocarcinoma, and this decrease correlated with mucin sulfation. In summary, the synthesis of less abundant, sialylated, fucosylated and extended, unbranched core 1 structures should be facilitated in the malignant cells. This is the first report of glycosyltransferase changes in human premalignant cells developing to tumourigenic cells. The data demonstrate that these cell lines are an excellent model to study the changes and regulation of mucin oligosaccharide biosynthesis during progression to cancer.
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PMID:O-glycan biosynthesis in human colorectal adenoma cells during progression to cancer. 802 Apr 79


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