c-myc Gene Effects on Cell Growth and Transformation
| Autor: | Erwin Fleissner, Vladimir Drozdoff, Louis Zeitz, Vincenzo Sorrentino |
|---|---|
| Rok vydání: | 1987 |
| Předmět: |
Cell division
etiology Nude Population Mice Nude Cell Transformation medicine.disease_cause General Biochemistry Genetics and Molecular Biology Cell Line Viral vector Proto-Oncogene Proteins c-myc Proto-Oncogene Proteins p21(ras) Experimental Mice History and Philosophy of Science Neoplasms Proto-Oncogene Proteins Proto-Oncogenes Cell Adhesion medicine Animals Cell Adhesion Cell Division Cell Line Cell Transformation Neoplastic chemically induced/genetics Cocarcinogenesis Fibroblasts drug effects/pathology/radiation effects Growth Substances pharmacology Mice Mice Inbred C3H Mice Nude Neoplasms etiology Proto-Oncogene Proteins c-myc Proto-Oncogene Proteins p21(ras) Proto-Oncogene Proteins genetics/physiology Proto-Oncogenes Recombinant Proteins physiology Tumor Stem Cell Assay Animals chemically induced/genetics Growth Substances education genetics/physiology Tumor Stem Cell Assay Mice Inbred C3H education.field_of_study Cocarcinogenesis Oncogene biology Cell growth General Neuroscience Neoplasms Experimental Fibroblasts Inbred C3H Recombinant Proteins Cell biology Cell Transformation Neoplastic drug effects/pathology/radiation effects Cell culture physiology biology.protein pharmacology Carcinogenesis Cell Division Platelet-derived growth factor receptor |
| Zdroj: | Annals of the New York Academy of Sciences. 511:329-337 |
| ISSN: | 1749-6632 0077-8923 |
| DOI: | 10.1111/j.1749-6632.1987.tb36261.x |
| Popis: | Epidemiological surveys of occurrence of human neoplastic disease as well as in-vitro and in-vivo experimental models indicate that tumorigenesis is a multistep process involving independent genetic events.1-3 In particular, studies with retroviruses and cloned oncogenes demonstrate that cooperation between oncogenes is required for full transformation of primary embryo cells in culture.4–8 Differences in response to growth factors can be observed between normal cells, which are capable of limited replication and are poorly transformable, and established cell lines, which can be more easily transformed by transfer of cloned oncogenes or exposure to carcinogens.9 Recent reports have provided evidence for effects of some oncogenes at specific points along biochemical pathways that regulate mitosis.10–13 For example, altered expression of the myc gene has been implicated in stimulation of cell growth in response to competence-inducing growth factors in normal cells and deregulation of cell growth in some neoplastic cells.14–16 Mouse C3H10T1/2 cells have been widely used in in-vitro transformation studies with chemicals and radiation.17,18 Several lines of evidence are suggestive of more than a single genetic event occurring before cells become able to overgrow the normal monolayer. 19–22 After carcinogenic treatment the appearance of foci of transformed cells is dependent upon proliferation of the initiated cell population, suggesting the requirement for a stochastic event in progression toward a transformed phenotype.23,24 Here we discuss results obtained by introducing the c-myc coding region via a murine retroviral vector into mouse C3H10T1/2 and rat F2408 cells. We observe that constitutive c-myc expression promotes growth in semisolid media and enhances responsiveness to PDGF, EGF, FGF, and TGF-β. Introduction of an exogenous c-myc gene into C3H10T1/2 does not result in cells that are tumorigenic. However, the expression of an exogenous myc gene increases the tumorigenicity of C3H cells carrying a mutated ras oncogene. We also observed that C3H10T1/2 cells expressing an exogenous myc gene are more efficiently transformed upon radiation or chemical carcinogen treatment. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text