Role of STAT3 decoy oligodeoxynucleotides on cell invasion and chemosensitivity in human epithelial ovarian cancer cells

Inflammation and Ovarian Cancer

“…The mechanism involves the inhibition of EMMPRIN, P-gp, and pAkt by STAT3 decoy ODN. These three proteins are probably the target proteins of STAT3 (Zhang, 2010). Increased levels of pSTAT3 are correlated with increased expression of HER-2/neu, EGFR and proliferation but not apoptosis markers.…”

Immunology and Immunotherapy of Ovarian Cancer

“…It was shown that EOC patients with depressive symptoms were characterized by IL-6 serum elevations [ 208 ]. IL-6-mediated STAT3 activation in EOC is responsible for tumor chemoresistance, as STAT3 antagonists were able to decrease EOC invasiveness and enhanced sensitivity to paclitaxel [ 194 ]. The mechanism of chemoresistance induction is probably mediated also by IL-6-dependent activation of apoptosis-inhibitory proteins [ 190 ].…”

“…The IL-23 and its receptor IL-23R have been engaged in carcinogenesis, and IL -23R gene polymorphism analysis revealed that the frequency of C and A alleles in rs10889677 position differed between EOC patients and controls, as well as between advanced and less-advanced tumors [ 194 ]. Ovarian cancer samples particularly showed high level of expression of genes encoding members and cooperates of TNF-signaling pathway, including IL-23, TGF-β, and NF-κB system [ 302 ].…”

Trojan Horses and Fake Immunity Idols: Molecular Mimicry of Host Immune Mediators by Human Cytomegalovirus

“…In a murine model of glioma, Stat3 has been demonstrated to promote an influx of macrophages, which correlated negatively with survival (Kong et al, 2010). In addition, Stat3 activation is associated with poor prognosis in ovarian cancer and considered a key factor in metastasis formation and chemo-resistance (Zhang et al, 2010). This is one of the most exciting new areas of research involving cmvIL-10, and additional studies are currently underway to define the role of cmvIL-10 in potentiating tumor progression.…”