Targeted inhibition of the JAK/STAT3 pathway inhibits ovarian carcinoma growth

ABSTRACT: Ovarian carcinoma (OC) is the fifth leading cause of death among women in the United States. Persistent activation of signal transducer and activator of transcription (STAT3) is frequently detected in OC. STAT3 is activated by Janus family kinases (JAK) via cytokine receptors, growth factor receptor and non-growth factor receptor tyrosine kinases. Activation of STAT3 mediates tumor cell proliferation, survival, motility, invasion, and angiogenesis, and recent work demonstrates that STAT3 activation suppresses anti-tumor immune responses and supports tumor-promoting inflammation. We hypothesized that therapeutic targeting of the JAK/STAT3 pathway would inhibit tumor growth by direct effects on OC cells and by inhibition of cells in the tumor microenvironment (TME). To test this, we evaluate

ORGANISM(S): Mus musculus

SUBMITTER: Denise Connolly 

PROVIDER: E-GEOD-63092 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress