Suppression of Egr-1 expression by siRNA abrogated the ability of TPA to induce Egr-1 and JNK-1 activities, moderately increasing the p21 activity and abrogating the anti-apoptotic effect of Egr-1 observed in the prostate cancer cell lines.
PC-3 and LNCaP prostate carcinoma cell lines were transiently transfected with wild-type Egr-1 expression plasmid (pCMV-Egr-1) and treated with cisplatin and TPA.
Furthermore, ionomycin (calcium ionophore) and TPA augmented the enhancer activity of PSME, implying that calcium is an important regulator for PSMA expression in prostate cancer cell.
In order to identify gene products associated with the development of acquired therapeutic resistance by prostate cancer cells, we created two novel apoptosis-resistant prostate cancer cell lines, LNCaP-TR (phorbol-ester [TPA]-Resistant) and LNCaP-SSR (Serum Starvation-Resistant) by repeated transient exposure of cultured human LNCaP cells to apoptotic stimuli followed by expansion of surviving cell populations.
Our data suggest that tumor suppressor genes involved in the oncogenesis of prostatic carcinoma may be localized between 8 pter and the PLAT locus and that additional/alternative tumor suppressor genes may be localized on chromosome 10 and on the long arm of chromosome 16 distal to the D16S4 locus.