High susceptibility of @entity1 XXXX cells to Fas-induced apoptosis is restricted to G1 phase of the cell cycle and can be increased by interferon treatment.

@entity1 @entity2800 @entity1778 @entity379 @entity2841 @entity3027
In this study, we analyzed the influence of cell cycle status manipulations of @entity1778 cells on Fas-mediated apoptosis using the @entity2841 -dependent @entity1 @entity2800 cell line AML-193 as a model. @entity2841 and long-term treatment with @entity379 ( @entity379 ) or interferon-alpha ( @entity3027 ) were used to manipulate the cell cycle status. Control cells were @entity2841 deprived, nonproliferating cells. @entity379 or @entity3027 treatment did not induce proliferation in control cells, but resulted in recruitment of cells from resting G(0) phase into activated G(1) phase. Using agonistic anti-Fas antibodies (FAS18), we demonstrated that this shift from G(0) to G(1) was accompanied by a 2.5-fold increase in Fas sensitivity. A similar increase in sensitivity to FAS18 could be obtained by induction of proliferation with @entity2841 . Quantitative FACS analysis of surviving cells after FAS18-induced apoptosis showed deletion of the G(1) compartment, but complete protection of resting G(0) cells. Cells in S or G(2)/M phase were relatively protected against Fas induction. In conclusion, sensitivity to Fas-mediated apoptosis was restricted to cells in G(1) phase of the cell cycle, and can be increased by treatment of cells with interferons. By this mechanism, interferon treatment may render @entity1778 cells more susceptible to lysis by T cells during immunotherapeutic interventions.
