Ial mode of therapy. The active elements of Anvirizel seem to become the cardiac glycosides oleandrin and oleandrigenin (see Smith et al., 2001). Anvirizel exerts its mechanism of action by interfering with specific membrane Na /K ATPase pumps, effectively inhibiting FGF-2 export (see Florkiewicz et al., 1998; Smith et al., 2001). The lack of extracellular FGF-2 brought on by Anvirizel prevents the CEACAM-5 Proteins Species activation on the FGF-2 signalling pathway, hence inhibiting prostate cancer cell proliferation in vivo in both PC-3 and DU-145 prostate cancer cells (see Smith et al., 2001); a related effect was observed in breast, lung, and melanoma cancer cells (see Smith et al., 2001; Manna et al., 2000; McConkey et al., 2000). As such, the FGF signalling axis is emerging as a clinically thrilling target of molecular intervention and justifiably warrants further exploration and targeted therapeutic development.Apoptosis players inside the prostateTransforming development factor-bIn the typical prostate, TGF-b inhibits epithelial cell proliferation and stimulates apoptosis, therefore acting in a tumour suppressor-like manner (see Bello-DeOcampo Tindall, 2003). TGF-b signal transduction is initiated by binding from the TGF-b ligand to two distinct cell surface receptors (TbRI and TbRII), both of which have serine/threonine kinase domains (see Bello-DeOcampo Tindall, 2003; Motyl Gajewska, 2004; Feng Derynck, 2005). Originally named for its ability to stimulate fibroblast development, TGF-b has proven to become a critical regulator of prostate cell development due to its ability to inhibit epithelial cell proliferation and induce apoptosis (see Massague et al., 1992; Zhu Kyprianou, 2005). TGF-b is released from prostatic stromal cells and exerts its impact in a paracrine manner, inhibiting prostatic epithelial cell development and inducing apoptosis (see Wu et al., 2001; Bhowmick et al., 2004). TbRII will be the principal receptor target for TGF-b, and upon binding, TbRII heterodimerizes with TbRI to initiate an intracellular signal transduction cascade (see Guo Kyprianou, 1999). TGF-b exhibits pleiotropy, and as such, the TGF-b signalling axis stimulates a wide array of downstream targets all of which have antiproliferative or apoptotic effects. As soon as the TbRI/TbRII heterodimer is formed, the serine/threonine kinase activity in the receptors is activated, effectively targeting the SMAD proteins because the main intracellular effectors of TGF-b signalling. Phosphorylation from the SMAD proteins, namely SMAD-2 and SMAD-3, initiates the transduction in the TGF-b signal in the cell membrane to the nucleus (see Massague, 1998; Motyl Gajewska, 2004). Upon nuclear translocation, the phosphorylated SMAD proteins trigger the activation of a series of transcription elements that dictate the proliferative and/or apoptotic outcomes of the cells (see Bello-DeOcampo Tindall, 2003). The transcription of Bax, a proapoptotic issue that deactivates that antiapoptotic aspect Bcl-2, is upregulated. Moreover, the SMAD-activated transcription things down-A.R. Reynolds N. KyprianouGrowth elements plus the prostateSregulate the transcription from the cell survival issue Bcl-2 (see Guo Kyprianou, 1999). Further, the cell cycle is properly halted by the elevated expression from the cyclindependent kinase inhibitor 3-Chloro-5-hydroxybenzoic acid Purity p27Kip1 (see Guo Kyprianou, 1999). Transcription activated by the TGF-b/SMAD signalling pathway leads to improved expression of IGFBP-3, the major binding protein involved in sequestering the p.