The murine Fc-gamma (Fcγ) receptor type II B1 is a tumorigenicity-enhancing factor in polyoma-virus-transformed 3T3 cells

Tal Zusman*, Ofra Gohar, Ilan Eliassi, Yechiam Avivi, Ellen Lisansky, Catherine Sautes, Jos Even, Christian Bonnerot, Wolf H. Fridman, Isaac P. Witz, Maya Ran

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review


The murine receptor for the Fc portion of IgG is a molecule expressed by cells of the immune system. This study suggests the hypothesis that Fcγ receptor type II B1 (FcyRIIB1) functions as a progression-enhancing factor when expressed ectopically on non-lymphoid tumor cells. It has been shown previously that BALB/c 3T3 cells transformed in vitro with polyoma virus (PyV) do not express FcγRII but acquire the expression of this receptor following an in vivo passage in syngeneic mice. The specific FcγRII transcript present in tumor cells was identified in this report as FcyRIIB1 (B1). In order to determine whether or not the ectopically expressed FcγRII plays a role in the progression of these transformed cells, PyV-transformed 3T3 cells were transfected with B1-cDNA. The B1 transfetted cells were tested for their ability to form local tumors in syngeneic mice, as compared to transfected cells which express the co-transfecting neomycine resistance (neo(res)) DNA alone or together with the locZ gene. FcyRIIB1 expressors exhibited a significantly higher tumorigenic phenotype than FcR-negative controls, though both types of cells exhibited the same growth curve in vitro. The ability of FcyRIIB1 to act as a potentially tumorigenicity-enhancing factor was also demonstrated as FcγRII was expressed by tumor cells, originating from inoculated FcyRIIB1-transfected cells, or from inoculation of a mixture of receptor-positive and negative cells. B1 expressing cells dominated the tumor-cell population over non-expressors. This dominance strengthened the hypothesis that FcR plays a role in tumor progression in vivo.

Original languageEnglish
Pages (from-to)221-229
Number of pages9
JournalInternational Journal of Cancer
Issue number2
StatePublished - 17 Jan 1996


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