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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.

journal_name

Oncogene

journal_title

Oncogene

authors

Gao CL,Wang LC,Vass WC,Seth A,Chang KS

subject

Has Abstract

pub_date

1988-09-01 00:00:00

pages

267-73

issue

3

eissn

0950-9232

issn

1476-5594

journal_volume

3

pub_type

杂志文章

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