herbimycin has been researched along with Urinary-Bladder-Neoplasms* in 2 studies
2 other study(ies) available for herbimycin and Urinary-Bladder-Neoplasms
| Article | Year |
|---|---|
Inhibitors of anchorage-independent growth affect the growth of transformed cells on poly(2-hydroxyethyl methacrylate)-coated surfaces.
We have described a microplate colorimetric assay to quantitate anchorage-independent cell growth, using plates coated with an anti-adhesive polymer poly (2-hydroxyethyl methacrylate) (polyHEMA).We investigated whether this method could be applied to human cancer cells of epithelial origin. HAG-1, a non-tumorigenic human gall-bladder carcinoma cell line, and its pSVneo and c-H-ras transfectants, which are also non-tumorigenic, did not grow on a polyHEMA-surface. In contrast, the v-src transformant which produced tumors in nude mice and formed colonies in soft agar, was able to proliferate on the coated surface, suggesting that tumorigenicity of human cancer cells correlates with the ability to grow on a polyHEMA-coated surface. We report on the feasibility of this method as a screening system for inhibitors of oncogenic transformation. Herbimycin A and radicicol, which have been reported to block Src function, suppressed the growth of v-src-transformed NRK and HAG-1 cells on the non-adhesive polyHEMA-surface at concentrations significantly lower than on plastic. Differences in the inhibitory concentrations were not observed with KB cells, and cytotoxic agents such as adriamycin did not show any selectivity between the 2 surfaces. Growth of ras-transformed cells on the coated surface was selectively blocked by L-739,749, a farnesyltransferase inhibitor. The results demonstrate that compounds causing reversion of transformed cells to normal, hence, selectively inhibiting cell growth in anchorage-independent conditions, can be screened using this microtiter plate assay. Topics: Adenocarcinoma; Animals; Benzoquinones; Cell Adhesion; Cell Division; Cell Line, Transformed; Drug Screening Assays, Antitumor; Humans; Lactams, Macrocyclic; Lactones; Macrolides; Methacrylates; Mice; Neoplasms; Oligopeptides; Protein-Tyrosine Kinases; Quinones; Rifabutin; Tumor Cells, Cultured; Urinary Bladder Neoplasms | 1996 |
Morphology of ras-transformed cells becomes apparently normal again with tyrosine kinase inhibitors without a decrease in the ras-GTP complex.
Radicicol, an inhibitor of protein-tyrosine kinase, was found to cause morphological reversion of v-Ha-ras-transformed NIH3T3 fibroblasts and T24 human urinary bladder carcinoma cells that contain an activated ras mutation. The network of actin stress fibers was restored during the treatment with radicicol. A similar morphological change was observed with another protein-tyrosine kinase inhibitor, herbimycin A. Radicicol did not cause any changes in the proportion of the active GTP binding form of p21ras or its subcellular localization. These results rule out the possibility that the morphological reversion by radicicol is due to direct or indirect inhibition of the p21ras function. Cycloheximide and actinomycin D inhibited the morphological change by radicicol, suggesting that the induced transcription of a gene(s) followed by de novo protein synthesis is required for suppression of the transformed phenotype in ras-transformed cells by tyrosine kinase inhibitors. Topics: Animals; Antibiotics, Antineoplastic; Benzoquinones; Cell Line, Transformed; Enzyme Inhibitors; Genes, ras; Guanosine Triphosphate; Humans; Lactams, Macrocyclic; Lactones; Macrolides; Mice; Point Mutation; Protein Binding; Protein-Tyrosine Kinases; Proto-Oncogene Proteins p21(ras); Quinones; Reference Values; Rifabutin; Transformation, Genetic; Tumor Cells, Cultured; Urinary Bladder Neoplasms | 1995 |