The results demonstrated that Egr-1 acts as a key player in prostate tumor cell growth and survival, while p21 plays a key pro‑apoptotic role in LNCaP and PC-3 prostate carcinoma cell lines.
The transcription factor Early Growth Response-1 (EGR-1) is overexpressed in human prostate tumors and contributes to prostate cancer progression through an unknown mechanism.
It is suggested that these defects in the suppressor network allow for the unopposed induction of TGFbeta1 and fibronectin, which favor transformation and survival of prostate tumor epithelial cells, and explain the role of Egr1 in prostate cancer.
In many prostate tumors, the activity of the transcription factor EGR1 (early growth response gene 1) is elevated due to overexpression of EGR1 and/or downregulation of the co-repressor, NAB2.
Increased heparanase expression is caused by promoter hypomethylation and up-regulation of transcriptional factor early growth response-1 in human prostate cancer.
The induction of Egr1 by external stimuli is generally transient but appears to be sustained in some prostate tumor cell lines and tumors, suggesting that Egr1 stimulates tumor cell growth.