So, gastrointestinal tract could signify a pref erential chemoprevention target as a consequence of its greater exposure to unmetabolized bioactive curcumin from diet regime than other tissues. All these data not merely recommend that curcumin has massive potential in the prevention and therapy of cancer but additionally properly justify the utility of using curcumin as an anti tumor agent. To arrest or to destroy two weapons of curcumin It really is now obvious that numerous in the phytochemicals pref erentially inhibit the development of tumor cells by inducing cell cycle arrest or apoptosis. The anti tumor result of curcumin has also been attributed in portion towards the suppression of cell proliferation, reduction of tumor load and induction of apoptosis in numerous cancer models both in vitro and in vivo.
Curcumin inhibits several levels inside of transcriptional network to restrict cell proliferation. It induces p53 dependent apoptosis in various cancers of colon, breast, bladder, neuron, lung, ovary and so on, although the two p53 dependent and independ ent G2 M phase arrest by curcumin has been observed in colorectal cancer cells. Curcumin pro motes caspase 3 mediated cleavage of catenin, enzalutamide decreases catenin Tcf Lef transactivation capacity for c Myc and cyclin D1. In addition, it activates caspase 7 and cas pase 9 and induces polyadenosine five diphosphate ribose polymerase cleavage through the down regulation of NFB in several myeloma cells. Furthermore, curcu min inhibits EGFR activation, Src action and inhibits activity of some nuclear receptors. Curcumin inhibitory effects upon Cox two and cyclin D1, mediated via NFB, also restrict tumor cell growth.
Induction of G2 M arrest and inhibition of Cox 2 exercise by curcumin in human bladder cancer cells has also been reported. It induces colon cancer cell apoptosis by JNK dependent sustained phosphorylation of c Jun and enhances TNF induced prostate cancer cell apopto sis. In reality, curcumin induces apoptosis in the two androgen dependent and androgen independent prostate find more information cancer cells. On the flip side, in breast carcinoma cells, it inhibits telomerase activity as a result of human telom erase reverse transcritpase. In Bcr Abl expressing cells, G2 M cell cycle arrest, together with greater mitotic index and cellular as well as nuclear morphology resembling individuals described for mitotic catastrophe, was observed and preceded caspase 3 activation and DNA fragmentation top to apoptosis.
Curcumin arrested cell growth in the G2 M phase and induced apop tosis in human melanoma cells by inhibiting NFB activa tion and hence depletion of endogenous nitric oxide. Yet, in mantle cell lymphoma curcumin continues to be uncovered to induce G1 S arrest

and apoptosis. In T cell leukemia curcumin induced development arrest and apoptosis in association with the inhibition of constitutively active Jak Stat pathway and NFB.