title: The role of v-mos in transformation, oncogenicity, and metastatic potential of mink lung cells.
abstract: A cloned line of S + L- mink lung cells (A clone), which exhibited a flat morphology, was superinfected with a novel dual-tropic virus (E1BX-MuLV) showing a broad host range and a B-tropism. These cells gave rise to transformed cells with two phenotypes: those which were still anchorage-dependent (AD), and those which readily detached spontaneously from the substratum and grew in suspension. A clone of these AD cells (B clone) was isolated and compared with a clone of the anchorage-independent suspension-cultured (AISC) cells (C clone). While the C clone exhibited a high oncogenicity and ability to metastasize in nude mice, the A and B clones were not tumorigenic. The integrated v-mos was greatly amplified in the C clone, and moderately increased in the B clone as compared with the A clone. The amounts of v-mos mRNA expressed by B and C clones paralleled those of v-mos sequence in their chromosomal DNA, whereas there was no detectable v-mos mRNA in the A clone. Thus, conversion of S + L- mink cells from an AD growth to an AISC phenotype accompanied by manifestation of oncogenicity and metastatic potential in nude mice is associated with amplification of integrated v-mos gene and its enhanced expression. Furthermore, a revertant (D clone) showing AD phenotype was derived from the C clone by selective growth in ouabain. This revertant exhibited a markedly decreased oncogenicity in nude mice, although the copy numbers of integrated v-mos gene and its mRNA did not differ from those of the parent C clone. While more p37mos protein was found in the C than in the D clone, it was not detectable in the A and B clone. The amounts of helper virus-related mRNA and infectious E1BX-MuLV were markedly higher in the B than in the C and D clones. It is concluded that v-mos gene amplification and overexpression is necessary for these cells to exhibit oncogenicity, but other factors associated with ouabain-resistance can modify or suppress its oncogenicity despite the v-mos amplification and mRNA overexpression.
authors.affiliation: Laboratory of Cellular Oncology, National Cancer Institute, NIH, Bethesda, Maryland 20892.
authors.forename: C L
authors.initials: CL
authors.lastname: Gao
authors.forename: L C
authors.initials: LC
authors.lastname: Wang
authors.forename: W C
authors.initials: WC
authors.lastname: Vass
authors.forename: A
authors.initials: A
authors.lastname: Seth
authors.forename: K S
authors.initials: KS
authors.lastname: Chang
mesh_terms: D000818:Animals; D002460:Cell Line; D002471:Cell Transformation, Neoplastic / Q000473:pathology*; D002472:Cell Transformation, Viral; D005814:Genes, Viral; D009052:Leukemia Virus, Murine / Q000502:physiology; D008168:Lung; D051379:Mice; D008819:Mice, Nude; D008907:Mink; D009362:Neoplasm Metastasis; D009374:Neoplasms, Experimental / Q000209:etiology / Q000473:pathology; D017232:Oncogene Proteins v-mos; D009857:Oncogenes; D010641:Phenotype; D012191:Retroviridae Proteins / Q000502:physiology*
chemical_list: D017232:Oncogene Proteins v-mos; D012191:Retroviridae Proteins