Figure 9 Comparision of chang in expression of apoptosis related genes as fold change (ratio of target:reference gene) in MCF-7 cells after 48 hours of exposure of 150 μg/mL of catechin. Figure 10 Comparision of chang in expression of apoptosis related genes as fold change (ratio of target:reference gene) in MCF-7 cells after 48 hours of exposure of 300 μg/mL of catechin. Discussion The mechanism of action of many anticancer drugs is based on their ability to induce apoptosis [19, 20]. There

are many mechanisms through which apoptosis can be enhanced in cells. Agents suppressing the proliferation of malignant cells by enhancing apoptosis may constitute a useful mechanistic approach to both cancer chemoprevention and chemotherapy. However, unfavorable side effects and resistance of MRT67307 solubility dmso many of the anticancer agents that have been developed are serious SB-715992 problems [21]. Thus, there is a growing interest in

the use of plant-based compounds to develop safe and more effective therapeutic agents for cancer treatment [22]. Because the side effects of green tea are modest and well tolerated [23], increasing attention is being given to the application of tea catechins for cancer prevention and treatment. EGCG conjugated with capric acid has been shown to be the catechin that most potently induces apoptosis in U937 cells. C10 has been shown to enhance apoptosis in human colon cancer (HCT116) cells [24]. Catechin compounds have been shown to exhibit cytostatic properties in many tumor models [2, 3]. Babich et al. (2005) found that catechin and epicatechin (EC) are less toxic Fludarabine chemical structure than other catechin compounds, selleck compound including ECG, CG, EGCG and EGC, in HSC-2 carcinoma cells and HGF-2 fibroblasts[25]. Hence,

I was interested in identifying whether apoptosis was the mode of death for cancer cells treated with CH (the least toxic form). To do so, I sought to determine the role of CH in inhibiting cell growth and modulating the expression of caspases-3, -8, and -9 and p53. The data presented in this paper demonstrate a time- and dose-dependent inhibition by CH of MCF-7 human breast cancer cell proliferation. There are many mechanisms through which apoptosis can be induced in cells. The sensitivity of cells to any of these stimuli may vary depending on factors such as the expression of pro- and anti-apoptotic proteins. The mitochondrial apoptotic pathways and death receptor pathways are the two major pathways that have been characterized in mammalian cells. The mitochondria have a central role in regulating the caspase cascade and apoptosis [26]. Caspases have a central role in the apoptotic process in that they trigger a cascade of apoptotic pathways [27]. The release of cytochrome -c from mitochondria leads to the activation of procaspase-9 and then caspase-3 [26]. The activation of caspase-3 is an important downstream step in the apoptotic pathway [28].