By Natasha Kyprianou
This booklet specializes in the sensible importance of focusing on apoptosis for the therapy of prostate melanoma. New options at the demanding situations when it comes to the improvement of resistance through androgen-independent tumors are brought, when it comes to the contribution of anoikis and cross-talk of androgens with key progress issue signaling pathways. This quantity additionally presents insightful dialogue at the exploitation of the apoptotic and angiogenic synergism in the direction of entire eradication of prostate tumors. final yet no longer least, it contains reflections at the drug improvement problem in response to the research of information from current medical trials.
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Additional info for Molecular Exploitation Of Apoptosis Pathways In Prostate Cancer
The role the caspases play at both the commitment and execution phases of apoptosis, resulting in the controlled demolition of the cell, has recently led to a cascading exploitation and design of new therapeutic modalities for the treatment of advanced prostate cancer. In theory, caspases can be targeted at two levels: gene expression (gene therapy), and post-translationally (zymogen cleavage and caspase activation). Gene therapy directed at common downstream effectors caspase-3 and caspase-7 should bypass intracellular checkpoint genes that limit apoptosis, making the cell unable to escape its death (Fig.
1999). Restoration of PTEN activity in PTEN-deficient prostate cancer cell lines increases sensitivity to FADD-mediated caspase8-driven apoptosis, and facilitates BID cleavage allowing for cytochrome c release and subsequent mitochondrial apoptosis (Yuan and Whang, 2002). AKTs are activated by second messengers via phosphatidylinositol 3-kinases (PI3Ks), a phosphorylation event that is counterbalanced by the activity of PTEN phosphatases (Stern, 2004). , 2004). The ability of phosphorylated AKT to inhibit prostate cancer cellular apoptosis is the ultimate product of dynamic cross-talk between this effector and multiple other anti-apoptotic pathways, as shown in Fig.
AR gene mutations in hormone-refractory prostate cancer that confer increased functional activity in the presence of ligands imply that resistance to androgen ablation is due to increased or altered sensitivity of the androgen signaling axis to other growth regulatory mechanisms (Zhu and Kyprianou, 2008; Knudsen and Scher, 2009). During prostate tumorigenesis the balance between the proliferation-inducing and apoptosis-enhancing functions of the AR can be disturbed not only by its mutations/inactivation but also via its interactions with signaling pathways.