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Multinucleation in the Presence of Cytochalasin B by RNA Tumor Virus-transformed Cells¹

Department of Microbiology and Immunology, Eastern Virginia Medical School, Norfolk, Virginia 23501

RNA tumor virus-transformed cell cultures derived from rat, mouse, hamster, and mink were examined for their response to cytochalasin B (CB), and the expression of this marker was correlated with growth in soft agar and tumorigenicity in vivo. Continuous cell lines transformed and chronically infected with Moloney murine sarcoma-leukemia virus (M-MSV-MuLV) or Kirsten murine sarcoma-leukemia virus were extensively multinucleated when treated with CB. Similarly, nonproducer Moloney murine sarcoma virus- or Rous sarcoma virus-transformed cells multinucleated in response to CB treatment, whereas uninfected or murine leukemia virus-infected cells remained predominately binucleate under comparable conditions. Rat kidney or embryo cell cultures, one to two passages after infection with M-MSV-MuLV, were highly multinucleated following CB treatment and acquired the ability to grow in soft agar. Mouse 3T3 cell lines, newly infected with M-MSV-MuLV, exhibited a moderate degree of CB-induced multinucleation. CB-induced multinucleation was directly correlated with anchorage-independent growth for most of the cell lines tested. An exception was the Moloney murine sarcoma virus-transformed mink cells which multinucleated in response to CB treatment but were unable to proliferate in soft agar. CB-induced multinucleation was directly correlated with the tumorigenicity of M-MSV-MuLV-transformed rat cells in syngeneic animals. These results demonstrate that CB-induced multinucleation is a useful in vitro growth-related marker of cell transformation by RNA tumor viruses and, in addition, show that this parameter of cell transformation is closely correlated with anchorage-independent growth in vitro and tumorigenicity in vivo.

¹ This work was supported by Cancer Research Emphasis Grant R01CA19714 within the Virus Cancer Research Program of the National Cancer Institute.

² To whom requests for reprints should be addressed.

Received 6/11/80. Accepted 9/ 8/80.

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