Antiserum was affinity purified on an antigen Sepharose column

So far our discus sion thus obviously shows the involvement of the parent of genome, p53, in curcumin induced cancer cell apoptosis via cell cycle regulation. p53 independent pathways and curcumin It's supplier Blebbistatin obvious that curcumin can produce selective cancer cell killing in a p53 dependent manner, but reduced p53 expression or activity is associated with a selection of neo plastic transformations. Increasing reports are suggesting that curcumin may prevent cell-cycle progression or even apoptosis in a p53 independent way at the same time, espe cially within the cells that lack functional p53. Curcumin induces apoptosis in p53 null lung cancer cells. It causes melanoma cell apoptosis by activating caspase 8 and caspase 3 via Fas receptor aggregation in a FasL inde pendent fashion, blocks NF cell survival pathway and inhibits the apoptotic chemical XIAP. Curcumin stops cellular isopeptidases, and cause cell death inde pendently of p53 in Inguinal canal pairs of HCT and RKO 116 cells with differential p53 status. It improves the chemotherapy-induced cytotoxicity in p53 null prostate cancer cell line PC 3, via up-regulation of C and Cip1 EBP xpressions and suppression of NF service. It also induces apoptosis in numerous myloma cells by inhibiting IKK and NF activity. Research indicates that curcumin down manages NF and AP 1 activity in androgen-dependent and independent prostate cancer cell lines. Curcumin is a potent inhibitor of protein kinase C, EGF receptor tyrosine kinase and I kinase. Therefore, curcumin stops the oncogenes including c fos, c jun, c myc, NIK, MAPKs, ELK, PI3K, Akt, CDKs and iNOS. In con trast to the reports, studies by Collet et al. Implies that curcumin induces JNK dependent apoptosis of cancer of the colon cells and it can induce JNK dependent sus tained phosphorylation of c jun and stimulation supplier P22077 of AP 1 transcriptional activity. PKC can be inactivated by the oxidized form of cancer chemopreventive agent curcumin by oxidizing the vicinal thiols present within the catalytic domain of the enzyme. Recent studies indicated that proteasome mediated degradation of cell proteins play a pivotal role in the regulation of a few fundamental mobile proc esses including differentiation, proliferation, cell cycling, and apoptosis. It has already been shown that curcu min induced apoptosis is mediated through the ment of ubiquitin proteasome pathway. All these reports shows that curcumin can induce apoptosis or block cell cycle progression in a number of cancer cell lines, mostly via p53 dependent pathways, but it can also act in a p53 independent manner. Other functions of curcumin Curcumin prevents angiogenesis directly and via regula tion of angiogenic growth factors like vascular endothelial growth factor, basic fibroblast growth factor and epider mal growth factor, together with the genes like angiopoietin 1 and 2, hypoxia inducible factor 1, heme oxygenase 1, and the transcriptional factors like NF.