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Titolo:
Integrated viral genomes can be lost from adenovirus type 12-induced hamster tumor cells in a clone-specific, multistep process with retention of theoncogenic phenotype
Autore:
Pfeffer, A; Schubbert, R; Orend, G; Hilger-Eversheim, K; Doerfler, W;
Indirizzi:
Univ Cologne, Inst Genet, D-50931 Cologne, Germany Univ Cologne Cologne Germany D-50931 nst Genet, D-50931 Cologne, Germany
Titolo Testata:
VIRUS RESEARCH
fascicolo: 1, volume: 59, anno: 1999,
pagine: 113 - 127
SICI:
0168-1702(199901)59:1<113:IVGCBL>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
NUCLEOTIDE-SEQUENCE; FOREIGN DNA; MESSENGER-RNAS; MAMMARY-TUMORS; EARLY REGION-4; GENE; SITES; METHYLATION; EXPRESSION; POLYMERASE;
Keywords:
integrated adenovirus DNA; revertants of Ad12-induced tumor cells; single-cell cloning; PCR; clone-specific pattern of loss of Ad12 DNA;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Doerfler, W Univ Cologne, Inst Genet, Weyertal 121, D-50931 Cologne, Germany Univ Cologne Weyertal 121 Cologne Germany D-50931 ne, Germany
Citazione:
A. Pfeffer et al., "Integrated viral genomes can be lost from adenovirus type 12-induced hamster tumor cells in a clone-specific, multistep process with retention of theoncogenic phenotype", VIRUS RES, 59(1), 1999, pp. 113-127

Abstract

In adenovirus type 12 (Adl2)-induced tumor cells, in Adl2-transformed cells and in continuously passaged cell lines from these sources, the viral DNAis integrated in multiple copies, usually at a single chromosomal location. In different tumors or cell lines, the sites of integration of Ad12 DNA are all different. Rare exceptions exist. In most instances, the integrated viral DNA resides very stably in, the host cell genomes. However, upon continuous serial passage of such cell lines, the integrated viral DNA can be destabilized and lost. In two instances, i.e. in the Adl12-induced hamster tumor cell lines H1111(1) and CLAC1, we have investigated the loss of integrated viral DNA in detail. After extended serial passage, these two cell lines seemed to be devoid of Ad12 DNA sequences, as detectable by Southern blot hybridization, but continued to induce tumors after reinjection into hamsters. Cells from these two cell lines were now recloned three times, and DNAs from cultures derived from several individual clones were reinvestigatedfor the presence of several parts of the viral genome by the polymerase chain reaction (PCR). Some of the clones still carried parts of the Ad12 genome. However, several clones were isolated that proved free of all parts of the viral genome, except for minute segments from the right terminus of theAd12 genome. Apparently, the loss of integrated viral DNA from these cell lines proceeded as a continuous, gradual, multistep process whose pattern could differ from cell clone to cell clone, once destabilization had been initiated. The mechanism of destabilization is not understood. Cell populations of 2 x 10(6) to 3 x 10(7), and as low as 10(2), cells from the clones, that contained only minimal remnants from the right viral DNA terminus, werereinjected into newborn or 13-20 day-old weanling Syrian hamsters (Mesocricetus auratus). Tumors developed within 5-17 days after injection. Tumor cell clones also grew in soft agar. The injection of primary hamster skin fibroblasts never elicited tumor formation. The tumor cells induced by this reinjection proved repeatedly free of Ad12 DNA both by Southern blot hybridization and by PCR, except for those cell and tumor clones that contained small segments of the right terminal E4 region of the Ad12 genome. The tumor cells, however, retained their oncogenic phenotype. The results raise questions about the cell clone-specific excision patterns of integrated foreign DNA from the recipient genome and the possibility of a hit-and-run mechanismof adenoviral oncogenesis. (C) 1999 Elsevier Science B.V. All rights reserved.

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Documento generato il 09/07/20 alle ore 20:02:29