Thus, SLFN5 is both an IFN-stimulated response gene and a repressor of IFN-gene transcription, suggesting the existence of a negative-feedback regulatory loop that may account for suppression of antitumor immune responses in glioblastoma.
Knockdown of STAT1 expression mimicked the effect of overexpression of miR203 in glioblastoma cell lines, and inhibited cell proliferation and migration, increased sensitivity to apoptosis induced by IFN or temozolomide in vitro, and inhibited glioblastoma tumorigenesis in vivo.
We analyzed 19 samples of various astrocytic tumors (3 astrocytomas, 5 anaplastic astrocytomas, and 11 glioblastomas) for loss of heterozygosity (LOH) on chromosome 9p at 6 microsatellite loci (D9S54, IFNA, D9S171, D9S104, D9S165, and D9S166).
To investigate the biological effects of class I IFN gene transfer and constitutive expression in glioblastoma cells devoid of this gene cluster, the authors have developed a stable IFNalpha "transfectant" of the cell line U118.