Stat a potent inhibitor of the enzyme Raloxifene Estrogen/progestin receptor inhibitor activity t of HDAC6 is, it m Possible that the reduction belinostat induced mutant p53 expression by a reduced dependence Dependence of Hsp90 as a result of drug-induced inhibition HDAC6 is caused. In accordance with the involvement of HDAC6 in this process, we found that selective HDACi compounds that do not HDAC6 inhibitory activity T are not easy to reduce the expression of the mutated p53 in DU145 cells. However, we have not generated the experimental data support the involvement of Hsp90 in this process. Additionally Tzlich to mutated p53 is reduced another potentially oncogenic protein whose expression by belinostat in prostate cancer cells is the transcription factor ERG. As previously mentioned HNT, are gene mutations lead to overexpression of the ERG common in prostate cancer and appear to be associated with aggressive disease. Interestingly, a high expression of HDAC1 has recently with prostate cancer overexpressing ERG, produced 29 leadingthe authors of this study in combination suggest that prostate cancer may benefit from positive ERG epigenetic therapy with HDACi. In addition, the ERG has been shown to indirectly show with HDAC1.30 belinostat We, here reduces the expression of proteins ERG online prostate cancer cells expressing a fusion protein of the ERG gene contains lt This finding is consistent with the previously established connection between ERG and HDACs with the suggestion that HDACi can be particularly effective against tumors positive ERG. In parallel to the negative regulation by the protein in cells belinostat ERG provides VCAP, also detected a simultaneous erh Increase the expression of p21 as a result of drug Water treatment. The p21 protein was placed in the inhibition of the cell cycle in compound and has been shown to be induced by belinostat and other HDACi.1 3, the relative Posts GE, if any, that the reduced expression of proteins that could potentially oncogenic as ERG make and mutated p53, and one obtains Hten expression of proteins such as p21 growthinhibitory the m for may have with the general growthinhibitory / cytotoxic activity t of belinostat on a cell line that showed particular is unknown. While it may be that the activity T growthinhibitory / cytotoxic belinostat most cancer cells through a trailer Ufung molecular Ver Changes, as described above, the M Possibility that a dominant Ver Change belinostat molecular catastrophic induced which is primarily responsible, is of the shops fts by a variety of cancer cell lines, can not be excluded. In the latter scenario identified many molecular mediation belinostat Ver Changes can k In fact, unnecessary wear and shows little growth inhibitory or cytotoxic activity of t this connection that most cancer cells. However, although this scenario is correct, then this belinostat influence of several panels, the independent Ngig inhibit the growth of cancer cells may be advantageous as a means of providing EUR ack up The mechanisms uct and to the death Adriamycin Topoisomerase Inhibitors of cancer cells to weight. Since belinostat and other compounds HDACi more independent Independent pathways in the growth and / or the survival of influence involved in cancer cells, it may be more difficult for tumor cells to innate resistance sentieren pr Or acquire resistance to these agents compared to connections.