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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of cancer research and clinical oncology 126 (2000), S. 595-600 
    ISSN: 1432-1335
    Keywords: Key words Liver cancer ; Tumor metastasis ; Adhesion ; β Peptide ; Intercellular adhesion molecule-1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Purpose: To study the inhibitory effects of synthetic β peptide on invasion and metastasis of liver cancer. Methods: Membrane-type intercellular adhesion molecule-1 (ICAM-1) expression of SMMC-7721 cultured hepatoma cells (7721 cells) was detected by immunofluorescence cell flowmeter. The adhesion of 7721 cells to fibronectin (FN) was assayed by the MTT method. The adhesion of 7721 cells to 7721 cells, 7721 cells to endothelial cells, and 7721 cells to lymphocyte cells was detected by adhesion assay. LCI-D20 human liver cancer metastasis model in nude mice was used in this experiment. One hundred micrograms of β peptide per mouse were injected subcutaneously after tumor was resected premetastatically or postmetastatically to observe its effect on liver cancer metastasis after hepatectomy. Results: Membrane-type ICAM-1 expression of SMMC-7721 cells treated by β peptide was lower than that of the untreated cells. The adhesion of 7721 cells to FN, 7721 cells to 7721 cells, 7721 cells to endothelial cells, and 7721 cells to lymphocyte cells was also lower in the β peptide group than in the untreated group. Conclusions:β Peptide can block the adhesion of 7721 cells to FN, 7721 cells to some host cells in vitro, and inhibit HCC metastasis of LCI-D20 model posthepatectomy in vivo, so it could potentially act as an anti-metastasis drug.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1617-4623
    Keywords: Key words Yeast ; Cell Cycle ; Checkpoints ; DNA damage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Chk1 is an evolutionarily conserved protein kinase that plays an essential role in mediating G2 arrest in response to DNA damage in Schizosaccharomyces pombe and human cells. It functions by maintaining the inhibition (by phosphorylation of a specific tyrosine residue) of the cyclin-dependent kinase Cdc2 that initiates the G2/M transition. Here, we characterize a structural homologue of Chk1 in the budding yeast Saccharomyces cerevisiae. In this organism, G2/M arrest following DNA damage is considered to be independent of tyrosine phosphorylation of the Cdc2 homologue Cdc28. Nevertheless, a partial defect in G2/M-phase arrest following treatment with ionizing radiation, but not UV radiation, is associated with deletion of CHK1. The fact that such an effect remains detectable in cells synchronized with the microtubule inhibitor nocodazole prior to γ irradiation implies the existence of a CHK1-dependent checkpoint in M phase. We conclude from epistasis analysis that Chk1 participates in the Pds1-dependent subpathway of M-phase arrest. In spite of the partial checkpoint defect of the chk1 mutant, the survival of colony-forming cells is not notably decreased following UV and γ irradiation. In two-hybrid screens, we identified a heme-binding stress protein (encoded by the yeast ORF YNL234W), a protein involved in genomic silencing (Sas3) and Chk1 itself as interacting partners of Chk1.
    Type of Medium: Electronic Resource
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