butyrolactone-i and Fibrosarcoma

butyrolactone-i has been researched along with Fibrosarcoma* in 2 studies

Reviews

1 review(s) available for butyrolactone-i and Fibrosarcoma

ArticleYear
[CDK and MMP inhibitors].
    Gan to kagaku ryoho. Cancer & chemotherapy, 1997, Volume: 24, Issue:11

    CDK inhibitor, Butyrolactone I inhibited CDK1, 2 and 5 in CDKs. In syncronized human lung fibroblast WI38 cells, it inhibited G1/S transition by inhibiting the phosphorylation of RB protein and G2/M transition by inhibiting the phosphorylation of H1 histone. Also, it selectively inhibited the initiation of DNA replication. The MMP inhibitor, BE16627B, reversively inhibited metalloproteinases including MMPs. It showed the MMP-dependent inhibition of the growth and metastasis of human tumor cells in nude mice without any cytotoxicity and severe side effects. The MMP inhibitor, Marimastat, showed remarkable prolongation of the life span of patients with pancreatic tumors in clinical trials.

    Topics: 4-Butyrolactone; Animals; Antineoplastic Agents; Colonic Neoplasms; Cyclin-Dependent Kinases; Dipeptides; Doxorubicin; Enzyme Inhibitors; Fibrosarcoma; Humans; Metalloendopeptidases; Mice; Mice, Nude; Protease Inhibitors; Succinates

1997

Other Studies

1 other study(ies) available for butyrolactone-i and Fibrosarcoma

ArticleYear
Cell cycle control with minimal participation of Cdk2 in a murine fibrosarcoma clone cultured in protein-free medium.
    Biochemical and biophysical research communications, 1997, Mar-27, Volume: 232, Issue:3

    The differences in the protein expression of cyclins, cyclin-dependent kinases (cdks), and their inhibitors and cdk kinase activities were examined in serum dependent (SD) and independent (PF) clones of the murine fibrosarcoma cell line, Gc-4. The expression of cyclin A in SD was minimal in contrast to PF. Furthermore, cdk2 kinase activity in PF was remarkably lower than that in SD, yet the G1/S transition in PF appeared normal. PF was also resistant against the selective inhibitor of cdk2, butyrolactone I. These findings suggest that tumor cell proliferation and tumor progression can be promoted by the activation of a molecule(s) downstream of cdk2.

    Topics: 4-Butyrolactone; Animals; CDC2-CDC28 Kinases; Cell Cycle; Cell Division; Cell Separation; Culture Media, Serum-Free; Cyclin-Dependent Kinase 2; Cyclin-Dependent Kinase 4; Cyclin-Dependent Kinases; Cyclins; Enzyme Inhibitors; Fibrosarcoma; Flow Cytometry; Mice; Protein Serine-Threonine Kinases; Proto-Oncogene Proteins; Tumor Cells, Cultured

1997