thereby reducing dysregulation of myocardial ionic homeostasis

These results not merely shown that the critical signaling events upon which cell fasudil concentration cycle progression depends occur during G1 phase in standard cells, but during G2 phase in actively growing cancer cells but also that G2 phase of cell cycle plays a critical role in preventing hyper proliferative status of cancer cell and is thus susceptible to effective anti cancer drug therapy. With sophisticated time-lapse movie micrography and quantita tive imaging method our works with breast malignant cells and adjacent non malignant cells suggest that curcu minute didn't alter the cell cycle progression of carcinoma cells, although it induced apoptosis in the exact same at G2 stage of cell cycle while reversibly blocking non malignant cell cycle progression without apoptosis. An interesting finding in this research was that curcumin seemed to Organism be sparing the typical epithelial cells by arresting them at the G0 phase of the cell-cycle via down regulation of cyclin D1 and its associated protein kinases or up regulation of the inhibitory protein. The findings with cyclin D1 deregulated cells showed that curcumin didn't change cyclin D1 expression level in cancer cells, but in standard cells, where cyclin D1 expression is tightly reg ulated by mitogenic signaling, its expression is inhibited by curcumin. This failure of curcumin to hinder cyclin D1 expression in cyclin D1 deregulated cells may possibly serve as the cornerstone for differential regulation of cancerous and nor mal cells. Additionally, curcumin was found to inhibit the association of cyclin D1 with CDK4CDK6 or phosphor ylation of pRb in a few cancer cells where the expression of cyclin D1 is not deregulated and therefore arrest them at G0 G1 phase. This yellow pigment has been shown to inhibit neoplastic cell proliferation by decreasing Cdk1 kinase activity and arresting cells at G2 M check point. TIC10 concentration Ectopically over-expression of cyclin D1 makes susceptibility of these cells towards curcumin toxicity. These results may explain why in cancer cells, despite up-regulation of p53 and increase in Cip1 level, there was no cell cycle arrest. Actually, the degree of cyc lin D1 is quite saturated in these cells and remained unchanged upon curcumin treatment. Ergo, the total amount of Cip1, as up regulated by curcumin, was still not adequate to over-power cyclin D1 and to avoid cell cycle progression. On the other-hand, in non-malignant cells, the level of Cip1 increased dramatically with parallel down regulation of cyclin D1, thus making the ratio of Cip1 to cyclin D1 1 and this might be one of the causes of cell-cycle arrest without apoptosis. The discussion not just applies curcumin activity with cell-cycle regulation but also describes the mechanism underlying the differential impact of the phytochemical in normal and malignant cells. Curcumin regulating guardian of genome The tumor suppressor gene p53, the guardian of genome acknowledged, is found in the crossroads of a net-work of signaling pathways which can be essential for cell growth regulation and apoptosis.