In our study performed by immunohistochemistry, 22 out of 46 glioblastomas (48%) were strongly positive for staining with a STAT-1 antibody, 9 (20%) showed an intermediate reactivity, 8 (17%) low immunoreactivity, and 7 (15%) were completely negative.
We studied the role of signal transducer and activator of transcription 1 or 5 (STAT(1) or STAT(5)) and Bcl-X(L) proteins in IN-induced proliferative inhibition on CML cells.
Both up-regulation of CD22 expression and immunoglobulin M (IgM) production, markers of CLL differentiation, were inhibited by a decoy oligonucleotide for STAT1, indicating that STAT1 is necessary for Bryostatin 1-induced differentiation of CLL cells.
Together, our results demonstrate that IFNalpha induces TRAIL expression via a STAT-1/IRF-1-dependent mechanism in human bladder cancer cells, and this induction of TRAIL plays an important role in IFNalpha-induced cell killing.
Furthermore, we show that targets of unphosphorylated STAT1, such as antigen presenting genes and CASP1, are also repressed by hypoxia possibly through the same STRA13-mediated mechanism.
Inhibition of the Rho GTPase pathway at the level of isoprenoid/cholesterol synthesis with mevastatin reduces PIAS1 expression, increases STAT1 activation, and restores NOS2 expression in models of CF epithelium, suggesting that pharmacological inhibition of the isoprenoid synthesis/Rho GTPase pathway may represent a potential avenue for therapeutic intervention for CF.
Moreover, phosphorylation of STAT-1 at tyrosine 701 is substantially reduced in both IFN-gamma-treated human choriocarcinoma and primary TBCs compared with HeLa cells or primary foreskin fibroblasts.
These results demonstrate the presence of STAT1-expressing TAM in FL and their association with an adverse outcome, thus emphasizing the relevance of non-tumor cells in the control of the growth and survival of lymphoma cells.