Further studies on the protein may help elucidate its role in prostate cancer progression. BASP1 is a Wilms’tumor suppressor protein -associated factor that can regulate WT1 transcriptional activity and it may be a potential target for prostate cancer therapy. TRIP13 is a thyroid receptor interacting protein whose gene shows copy number 
changes in 68% of 19 early stage NSCLC tumor samples. TRIP13 has also been implicated as a marker of early disease related mortality in multiple myeloma as part of a 70-gene model. It is surprising to note that annexin A2 was been previously reported to be upregulated in various tumor types with a role in cell migration, invasion and adhesion, but is downregulated in PC3-ML2 compared to PC3-N2 in our current study. Several studies have linked the overexpression of EphA2 to malignant progression. However, paradoxically, activation of EphA2 kinase on tumor cells can trigger signaling events that are more consistent with a tumor suppressor. These include inhibition of integrin signaling, Ras/ERK pathway, and Rac GTPase activation, which is correlated with inhibition of cell proliferation and migration. Furthermore, EphA2 has also been shown to be a target gene for p53 family of proteins and it causes apoptosis when overexpressed. Recent data supporting a tumor suppressor role of EphA2 include the demonstration that EphA2 is a key mediator of UV-induced apoptosis independent of p53, and the dramatically increase insusceptibility to skin carcinogenesis in EphA2 KO mice. Our current studies show a significant downregulation of EphA2 in the metastatic cells and future studies to determine how EphA2 may contribute to the progression of prostate cancer. In summary, we have identified several proteins including plectin and vimentin that may act as markers for prostate cancer disease progression. These proteins could potentially make significant contributions to the prediction of aggressive metastatic disease compared to non-metastatic primary tumors. In addition they could assist in developing better treatment strategies for the disease. Further studies are needed to uncover the mechanisms responsible for these proteins in the development and progression of prostate cancer. Arrested development is a form of dormancy in which metabolic activity is significantly depressed or even absent. It is a widespread strategy employed by many organisms, from prokaryotes to mammals, in response to unfavorable thermal, nutritional or hydration conditions. Dormancy encompasses the phenomena of diapause, quiescence or cryptobiosis, and can be associated with desiccation when long-term periods of metabolic arrest are needed for survival. Interestingly, however, recent studies suggest that the molecular pathways underlying the process of dormancy show important similarities among different organisms, in spite of their very different survival strategies. In fish, embryonic dormancy is the most widespread form of arrested development and is often associated with dehydration tolerance, which allows survival during transient or prolonged environmental hypoxia and anoxia. Three major forms of arrested development have been described for fish embryos: delayed WZ8040 hatching, embryonic diapause, and anoxia-induced quiescence. Diapause is very common among annual killifishes which inhabit ephemeral ponds in regions of Africa and South and Central America that MK-1775 experience annual dry and rainy seasons. In annual killifish, diapause may occur at three distinct developmental stages, diapause I, II and III, which appear to respond to different environmental cues for induction and breakage of dormancy. Studies on diapause II and anoxia-induced quiescence embryos of the annual killifish Austrofundulus limnaeus show that during diapause metabolism is supported using anaerobic metabolic pathways, regardless of oxygen availability.