Chronic inflammation plays an important role in the initiation and progression 
of various human diseases including benign prostatic hyperplasia or prostate 
cancer. Here we show that the proinflammatory cytokine interleukin-6 (IL-6) has 
prosurvival effects and chronically activates the Jak2/STAT3 signalling pathway 
in a model of benign prostatic hyperplasia (BPH-1). We demonstrate that the 
antiinflammatory cytokine transforming growth factor-beta1 (TGF-beta1), which 
also permanently activates its canonical signalling pathway through SMAD 
proteins in BPH-1 cells, modifies the effects of IL-6 on cell proliferation. 
Importantly, TGF-beta1 inhibits IL-6 signal transduction by decreasing the 
phosphorylation levels of STAT3. This effect is associated with decreased 
expression of Jak2 at both mRNA and protein levels. Moreover, we showed that 
TGF-beta1 inhibits IL-6-induced expression of the cancer-associated gene MUC1. 
These observations demonstrated a novel interaction between TGF-beta1 and IL-6 
signalling and suggested another mechanism of how defects in TGF-beta 
signalling, frequently associated with prostate pathologies, can contribute to 
the disruption of tissue homeostasis.