Interferon-γ InducesIceGene Expression and Enhances Cellular Susceptibility to Apoptosis in the U937 Leukemia Cell Line

Type I consensus interferon (CIFN) gene transfer into human melanoma cells up-regulates p53 and enhances cisplatin-induced apoptosis: implications for new therapeutic strategies with IFN-alpha

“…In fact, both IRF-1 and STAT1 have been shown to favor the induction of apoptosis by different stimuli, apparently by reg-ulating the expression of different members of the family of caspases responsible for the final steps of apoptosis execution. [32][33][34] Interestingly, induction of apoptosis following overexpression of p53 was found to be associated with activation of ICE-like proteases. 35 Ongoing studies will clarify whether the IFN-mediated enhancement of cisplatin sensitivity in the 8863 and 1B6 melanoma cells is dependent on an increase of caspase activity.…”

MyD genes in negative growth control

“…DNA damage-induced apoptosis in mitogen-activated mature T lymphocytes, which is p53 independent, was observed to be dependent on IRF-1. Ectopic expression of IRF-1 in mature T cells or U937 cells resulted in activation of the endogenous gene for caspase 1 (ICE), and enhanced the sensitivity of these cells to radiation-induced apoptosis (Tamura et al, 1995(Tamura et al, , 1996. It has been proposed that IRF-1 interacts with Signal Transducers and Activator of Transcription (STATs) to induce the expression of caspase genes (Kumar et al, 1997;Hoey, 1997).…”

Lack of IRF-1 expression in acute promyelocytic leukemia and in a subset of acute myeloid leukemias with del(5)(q31)

“…15,16 In addition to its role in growth suppression, IRF-1 plays a key role in both p53-dependent and p53-independent apoptosis, in part due to its regulation of Fas-antigen and interleukin-␤ converting enzyme (ICE) expression. [15][16][17][19][20][21] Thus, altered expression of IRF-1 may contribute to the neoplastic phenotype by compromising differentiation, growth regulation, or apoptosis.…”