Recent report showed that E-cadherin is a direct target of miR-92a and that the expression of miR-92a promoted lymph node metastasis of human esophageal squamous cell carcinoma via down-regulation of Ecadherin. Therefore, RANKL could also promote PCa progression via up-regulation of miR-92a and consequently by down-regulation of E-cadherin. Interestingly, isoflavone and BRDIM were able to attenuate the up-regulation of miR-92a stimulated by RANKL treatment, suggesting the importance of these natural agents in the inhibition of PCa progression and bone metastasis. In addition to the inhibitory effects on osteoclasts, isoflavone and BR-DIM also inhibted the differentiation of osteoblast with down-regulation of periostin, one of the important genes for osteoblast differentiation. Therefore, by targeting both osteoclast and osteoblast differentiation, isoflavone and BR-DIM could effectively interrupt bone remodeling, providing unfavorable micoenvironment for the homing of PCa cells to the bone. Although both isoflavone and BR-DIM showed inhibitory effects on bone cell differentation, the involved molecules and altered levels by isoflavone or BR-DIM treatment were not the same,(R)-(-)-Modafinic acid suggesting that complex regulatory mechanisms are involved. These results suggest the multi-targeting effects of isoflavone and BR-DIM, which will make isoflavone and BR-DIM powerful agents for inhibiting PCa growth in bone microenvironment. In conclusion, isoflavone and BR-DIM were able to target both osteoclast and osteoblast differentiation, and also could target multiple molecules in PCa cells; therefore, these agents could inhibit bone remodeling and PCa growth, suggesting that isoflavone and BR-DIM could be very useful for the prevention of PCa progression, especially bone metastasis. The biological activity of isoflavone and BR-DIM is mediated through the downregulation of In MS research, some quantitative proteomics studies have already been completed. Looking at 2D-DIGE experiments, mostly biomarker studies on human CSF were performed. In one proteomics study in MS research (-)-Tetramisole, a comparison between multiple plaque-types was performed to obtain new therapeutic targets, although not by 2D-DIGE. Post-mortem MS samples are often a snapshot of longstanding disease. Therefore, a well characterized homogeneous animal model, experimental autoimmune encephalomyelitis, was selected for this study to obtain a sample of the inflammatory lesions. Only 2 experiments were published in which CNS tissue of EAE animals was used for a 2D-DIGE study. In these studies protein expression was compared between two experimental groups. To get a better understanding of the pathomechanisms in MS and EAE, we decided to use experimental groups at different time points during the disease. Here we report disease stage-specific variations in brain protein expression found in samples from different time points during acute EAE, a well characterized animal model of MS. The brainstem of this model was selected to focus on CNS inflammatory pathways involved in the lesion development and regulation of EAE, as it was shown that disease related macrophage infiltration at the onset of acute Lewis rat EAE was mainly localized to the caudal part of the brainstem. We performed a 2D-DIGE study to quantitatively compare protein levels at different disease stages. Samples were obtained before onset of the symptoms, at the top of the disease and after recovery. This allows us to create graphs of brain protein levels over time. We were able to identify 75 unique proteins present in 92 differential gel spots. All of these proteins were analyzed with Ingenuity Pathway Analysis software to disclose connections between these proteins, and thus define pathways that could be involved in the molecular mechanisms of MS.