[Mechanism of proliferation of cells transformed by the Moloney mouse sarcoma virus after stable reversion to a non-malignant state].
Prolonged interferon (IFN) treatment can convert Moloney sarcoma-transformed mouse Balb C fibroblasts to a stable non-malignant status. The cells recover a number of differentiated features, which are maintained even when IFN is permanently omitted from the tissue culture medium. We show here that reversion could be at least in part attributed to constitutive IFN beta synthesized only in the reverted cells. The continued replication of these cells, although unable to induce tumours in athymic mice, could be the result of the maintained expression of an IFN antagonist termed sarcolectin (SCL), a balance being struck between the effects of v-mos oncogene, interferon beta and SCLs. In agreement with Lampl et al. [11], we suggest that normal cell growth is discontinuous, consisting of sudden bursts followed by prolonged arrests which could be necessary to promote differentiation during the ensuing interphase.
Chany
C
C
Université Pierre-et-Marie-Curie, Laboratoire de Physiologie Cellulaire, Paris, France.
Kaba
A
A
Jiang
P H
PH
Chany-Fournier
F
F
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D002472:Cell Transformation, Viral; D005347:Fibroblasts / Q000166:cytology; D007372:Interferons / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D037102:Lectins / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D008979:Moloney murine leukemia virus; D012008:Recurrence; D014407:Tumor Cells, Cultured / Q000166:cytology
D037102:Lectins; C039495:sarcolectin; D007372:Interferons