So, gastrointestinal tract could represent a pref erential chemoprevention target as a consequence of its greater publicity to unmetabolized bioactive curcumin from diet plan than other tissues. Every one of these knowledge not simply suggest that curcumin has tremendous possible during the prevention and therapy of cancer but also well justify the utility of making use of curcumin as an anti tumor agent. To arrest or to destroy two weapons of curcumin It is now apparent 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 component towards the suppression of cell proliferation, reduction of tumor load and induction of apoptosis in diverse cancer models each in vitro and in vivo.
Curcumin inhibits many ranges within transcriptional network to restrict cell proliferation. It induces p53 dependent apoptosis in diverse cancers of colon, breast, bladder, neuron, lung, ovary and so forth, whilst the two p53 dependent and independ ent G2 M phase arrest by curcumin is observed in colorectal cancer cells. Curcumin professional motes caspase three mediated cleavage of catenin, discover this decreases catenin Tcf Lef transactivation capacity for c Myc and cyclin D1. Furthermore, it activates caspase seven and cas pase 9 and induces polyadenosine 5 diphosphate ribose polymerase cleavage with the down regulation of NFB in a variety of myeloma cells. Additionally, curcu min inhibits EGFR activation, Src activity and inhibits exercise of some nuclear receptors. Curcumin inhibitory effects upon Cox 2 and cyclin D1, mediated by 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 fact, curcumin induces apoptosis in both androgen dependent and androgen independent prostate price SB-207499 cancer cells. On the flip side, in breast carcinoma cells, it inhibits telomerase exercise by human telom erase reverse transcritpase. In Bcr Abl expressing cells, G2 M cell cycle arrest, along with elevated mitotic index and cellular too as nuclear morphology resembling individuals described for mitotic catastrophe, was observed and preceded caspase 3 activation and DNA fragmentation primary to apoptosis.
Curcumin arrested cell growth on the G2 M phase and induced apop tosis in human melanoma cells by inhibiting NFB activa tion and so depletion of endogenous nitric oxide. Nevertheless, in mantle cell lymphoma curcumin has become noticed to induce G1 S arrest

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