alpha mannosidase/neoplasms

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Functionalized pyrrolidine inhibitors of human type II alpha-mannosidases as anti-cancer agents: optimizing the fit to the active site.

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Refining the chemical structure of functionalized pyrrolidine-based inhibitors of Golgi alpha-mannosidase II (GMII) to optimize binding affinity provided a lead molecule that demonstrated nanomolar competitive inhibition of alpha-mannosidases II and an optimal fit in the active site of Drosophila

Studies toward new anti-cancer strategies based on alpha-mannosidase inhibition.

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Changes in the glycosylation pattern of cellular glycoproteins constitute a hallmark in human cancer and influence tumor progression, suggesting that inhibitors of selected glycosidases may control cancer progression. Following the studies on swainsonine, a natural inhibitor of Golgi

Swainsonine, an alpha-mannosidase inhibitor, may worsen cervical cancer progression through the increase in myeloid derived suppressor cells population.

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Cervical cancer, caused by high oncogenic risk Human Papillomavirus (HPV) infection, continues to be a public health problem, mainly in developing countries. Using peptide phage display as a tool to identify potential molecular targets in HPV associated tumors, we identified α-mannosidase, among

Structure of Golgi alpha-mannosidase II: a target for inhibition of growth and metastasis of cancer cells.

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Golgi alpha-mannosidase II, a key enzyme in N-glycan processing, is a target in the development of anti- cancer therapies. The crystal structure of Drosophila Golgi alpha-mannosidase II in the absence and presence of the anti-cancer agent swainsonine and the inhibitor deoxymannojirimycin reveals a

Beta-galactosidase and alpha-mannosidase inhibit formation of multicellular nodules in breast cancer cell cultures.

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In response to an estrogen, confluent monolayers of MCF-7 cell cultures develop multi-cellular nodules, termed foci. Post-confluent development of foci occurs with physiologic levels of 17beta-estradiol and are inhibited by various anti-estrogens acting through either the estrogen or aryl

hMan2c1 transgene promotes tumor progress in mice.

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In order to study the biological significance of alpha-mannosidase Man2c1, hMan2c1 transgenic mice were developed. In 113 F0 mice, eight were found to be genomic PCR positive for hMan2c1; 9/20 (45%) F1 mice, 16/21 (76.2%) F2 mice, and 12/14 (85.7%) F3 mice were genomic PCR positive for hMan2c1.

Expression of L-PHA-binding proteins in breast cancer: reconstitution and molecular characterization of beta 1-6 branched oligosaccharides in three-dimensional cell culture.

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Expression of beta 1-6 branched oligosaccharides in human breast cancer cells was investigated in vivo and in vitro. Lectin histochemical and lectin blotting analyses of surgically resected specimens were performed using L-PHA (phaseolus vulgaris leukoagglutinin) lectin, which binds to beta 1-6

Inhibition of N-linked glycosylation by tunicamycin induces E-cadherin-mediated cell-cell adhesion and inhibits cell proliferation in undifferentiated human colon cancer cells.

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OBJECTIVE Aberrant protein glycosylation and disassembly of E-cadherin-mediated cell-cell adhesion are characteristics of epithelial cancer. However, the relationship between these two events in colorectal cancer remains to be defined. In this study, we analyzed whether N-glycan expression is

Functionalized pyrrolidines inhibit alpha-mannosidase activity and growth of human glioblastoma and melanoma cells.

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New substituted pyrrolidine-3,4-diol derivatives were prepared from d-(-)- and l-(+)-phenyl glycinol. The influence of the configuration and the substitution of the lateral side chain of these derivatives on the inhibition of 25 commercial glycosidases were determined.

The role of protein glycosylation inhibitors in the prevention of metastasis and therapy of cancer.

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Oligosaccharide moieties of cell-surface glycoproteins are thought to be involved in recognition events during cancer metastasis and invasion. Swainsonine, an inhibitor of the Golgi alpha-mannosidase II, has been shown to block pulmonary colonization by tumor cells and stimulate components of the

A long-wavelength fluorescent substrate for continuous fluorometric determination of alpha-mannosidase activity: resorufin alpha-D-mannopyranoside.

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A simple and reliable continuous assay for measurement of alpha-mannosidase activity is described and demonstrated for analysis with two recombinant human enzymes using the new substrate resorufin alpha-d-mannopyranoside (Res-Man). The product of enzyme reaction, resorufin, exhibits fluorescence

[Inhibition effect of Swainsonine on the growth and metastasis of gastric cancer in vivo].

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OBJECTIVE To study the immunomodulating effect of Swainsonine (SW), an inhibitor of alpha-mannosidase II, and the inhibiting effect on the growth and metastasis of gastric cancer. METHODS Nude mice with human gastric cancer xenograft orthotopically implanted into the gastric wall were fed with

Identification of the active site nucleophile in jack bean alpha-mannosidase using 5-fluoro-beta-L-gulosyl fluoride.

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Mannosidases play a key role in the processing of glycoproteins and thus are of considerable pharmaceutical interest and indeed have emerged as targets for the development of anti-cancer therapies. Access to useful quantities of the mammalian enzymes has not yet been achieved; therefore, jack bean

Carbonoyloxy analogs of the anti-metastatic drug swainsonine. Activation in tumor cells by esterases.

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Swainsonine (SW), a plant alkaloid and inhibitor of alpha-mannosidases, has been shown to inhibit N-linked oligosaccharide processing and to block tumor cell metastasis in mice. In this study, a series of SW analogs were chemically synthesized and compared for inhibition of complex-type N-linked

α-D-mannose derivatives as models designed for selective inhibition of Golgi α-mannosidase II.

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Human Golgi α-mannosidase II (hGM) is a pharmaceutical target for the design of inhibitors with anti-tumor activity. Nanomolar inhibitors of hGM exhibit unwanted co-inhibition of the human lysosomal α-mannosidase (hLM). Hence, improving specificity of the inhibitors directed toward hGM is desired in

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