The STAT3 is often dysregulated in genitourinary tumors. In prostate cancer, STAT3 activation correlates with Gleason score and pathological stage and modulates cancer stem cells and epithelial-mesenchymal transition. In addition, STAT3 promotes the progression from carcinoma in situ to invasive bladder cancer and modulates renal cell carcinoma angiogenesis by increasing the expression of HIF1α and VEGF. STAT3 is also involved in the response to tyrosine kinase inhibitors sunitinib and axitinib, in patients with metastatic renal cell carcinoma, and to second-generation androgen receptor inhibitor enzalutamide in patients with advanced prostate cancer. In this review, we describe the role of STAT3 in genitourinary tumors, thus describing its potential for future therapeutic strategies. Regulation of the protein STAT3 is often dysfunctional in genitourinary tumors, including prostate, bladder and kidney cancer. STAT3 is involved in the generation of these tumors and has an effect in their response to treatments. In this review, we describe its role in genitourinary tumors and discuss its potential for use in future therapies.
- drug resistance
- genitourinary tumors
- signal transducer and activator of transcription 3
- tumor microenvironment
ASJC Scopus subject areas