title: Establishment and characterization of clonal cell lines derived from a fibrosarcoma of the H2-K/V-JUN transgenic mouse. A model of H2-K/V-JUN mediated tumorigenesis.
abstract: We used fibrosarcoma from an H2-K/V-JUN transgenic mouse to derive a series of three immortal cell lines (JUN-1, -2, and -3). The cell lines exhibit strikingly different behavior regarding phenotype transformation. Features examined include contact inhibition and density limitation of growth, proliferation, invasiveness, motility, and organization of the microfilament system. Overall, JUN-2 and JUN-3 represent extreme phenotypes, with JUN-2 having a phenotype indicative of low-level cellular transformation and JUN-3 meeting all the criteria of the transformed phenotype. JUN-1 cells can also be regarded as transformed, but to a lesser extent than JUN-3. Their phenotype is in the majority of characteristics intermediary between JUN-2 and JUN-3. The transformation status is inversely related to the expression of the V-JUN transgene, which is the highest in JUN-2, lower in JUN-1 and very low in JUN-3. This might be related to the MHC class I promoter driving its expression and to the general observation of repression of MHC class I genes coupled with cellular transformation. Based on this premise, we present a model of H2-K/V-JUN-mediated tumorigenesis, in which v-jun-conditioned transformation represents merely an initial phase of tumorigenesis. Later during tumor progression, additional oncogenes are activated and/or tumor suppressor genes inactivated, leading on the one hand to further exacerbation of the transformed phenotype, and on the other hand to the repression of the H2-K/V-JUN transgene (fixed in JUN-3). We believe that the system of JUN cell lines can be valuable for further molecular analysis of transformation-related traits.
authors.affiliation: Department of Biology, Faculty of Medicine, Charles University, Pilsen, Czech Republic. jiri.hatina@lfp.cuni.cz
authors.forename: Jirí
authors.initials: J
authors.lastname: Hatina
authors.forename: Lucie
authors.initials: L
authors.lastname: Hájková
authors.forename: Jan
authors.initials: J
authors.lastname: Peychl
authors.forename: Emil
authors.initials: E
authors.lastname: Rudolf
authors.forename: Jindrich
authors.initials: J
authors.lastname: Fínek
authors.forename: Miroslav
authors.initials: M
authors.lastname: Cervinka
authors.forename: Josef
authors.initials: J
authors.lastname: Reischig
mesh_terms: D000199:Actins / Q000737:chemistry; D000818:Animals; D002455:Cell Division; D045744:Cell Line, Tumor; D002465:Cell Movement; D002471:Cell Transformation, Neoplastic; D005354:Fibrosarcoma / Q000473:pathology*; D016758:Genes, jun / Q000502:physiology; D006183:H-2 Antigens / Q000235:genetics* / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D009361:Neoplasm Invasiveness
chemical_list: D000199:Actins; D006183:H-2 Antigens; C024755:H-2K(K) antigen; C032876:H-2Kb protein, mouse