Special STAT3 inhibitor S3I-201 diminished the discrepancy of growth, metastasis and self-renewal ability between lnc-DILC-overexpression BC cells and their control cells, which further confirmed that STAT3 was acquired for lnc-DILC-disrupted BC cell growth, metastasis and self-renewal.
Retinoic Acid-Related Orphan Receptor C Regulates Proliferation, Glycolysis, and Chemoresistance via the PD-L1/ITGB6/STAT3 Signaling Axis in Bladder Cancer.
Further studies showed that estrogen receptor 1 (ESR1) increased the expression of miR-4324 by binding to its promoter, while the downregulation of ESR1 in BCa was caused by hypermethylation of its promoter. p-STAT3 induced the enrichment of DNMT3B by binding to the ESR1 promoter and then induced methylation of the ESR1 promoter.
Collectively, the present study demonstrated that PLCε may regulate glycolysis through the STAT3/LDHA pathway to take part in the development of human UBC.
Overall, the present study suggested that phosphorylated STAT3 may be a potential biomarker to predict radioresistance and tumor recurrence in patients with BCa following conventional radiotherapeutic intervention.
Cell cycle-defective phosphomimetic p27T157DT198D (p27CK-DD) activates STAT3 to induce a TWIST1-dependent EMT in human mammary epithelial cells and increases breast and bladder cancer invasion and metastasis.
Despite accumulating evidence suggesting a critical role of signal transducer and activator of transcription 3 (STAT3) and Survivin in human bladder cancer, the effects of silencing these genes on the proliferation of T24 bladder carcinoma cells remain unknown.
Furthermore, blocking Stat3 activity with the chemical inhibitor Stattic inhibited CXCL12-triggered Stat3 phosphorylation and cell invasion in T24 cells, suggesting that Stat3 activation is required for CXCL12 function in the mobility of bladder cancer.
In the present study, we tested the consequences of STAT3 inhibition in EGFR inhibitor-resistant head and neck squamous cell carcinoma (HNSCC) and bladder cancer models to determine whether STAT3 blockade can enhance responses to EGFR targeting.