ing ACCA, and the ability of MCF-7, T47D and MDA-231 cells to form colonies was monitored over the next 21 days. Our results show that in the absence of any ACCA, MCF-7, T47D and MDA-231 cells cells have a robust ability to form colonies and that ACCA inhibits this in a dose-dependent manner in all three tumor cell lines. A significant inhibitory effect of ACCA on breast cancer cells colony formation is apparent at even 25 mM doses of ACCA and with a 200 mM dose, the ability of breast cancer cells to form colonies is completely blocked. These results extend our previous observations indicating that that ACCA caused inhibition of cell death at a concentration greater than 25 mM and suggest that ACCA is a potent suppressor of cell growth. ACCA Affects Breast Cancer Cell Growth loss was observed upon treatment, suggesting that ACCA was well tolerated at this dose regimen. Discussion Although treatment of breast cancer has improved considerably, curative therapy is not available for these patients. Unfortunately, the treatments in use today, such as surgery, radiation and chemotherapy, are exhaustive to the patients. There’s therefore great need to focus on new treatments that 10336542 are effective in fighting specifically the tumors. Breast cancer, as almost malignant tumors, harbors aberrant metabolic pathways which support rapid cell proliferation and provide a growth advantage over normal cells. Previous 
finding suggest that lactate, the end of product of glycolysis, is produced in large amount in tumors and is more effective than glucose in the tumor cell energy metabolism under Tangeretin site aerobic conditions. The mechanism set forward involves a competition between lactate and glucose metabolism for the intracellular NAD+pool. In this context, it was shown that the main mechanism underlying this metabolic change include important cytotoxic and cytostatic effects on several human tumors including breast carcinomas. Additionnally, the loss of the reserve capacity of the mitochondrial function in breast cancer cells often leads to cell death via mitochondrial apoptotic signaling pathways. Because MCTs are key players in this process, disruption or alteration of the metabolism of tumor cells via inhibition of MCTs function represent promising therapeutic perspectives for the development of targeted therapies in breast cancer. In this study, we document the antibreast carcinoma and apoptosis-promoting properties of ACCA. On the basis of the previously confirmed genetic defects in the human tumor cell lines analyzed, including mutations p53, it is evident that the antineoplastic effect of ACCA, acting through MCT1, does not depend on the action of this tumor suppressor gene that is frequently altered in human cancers. The capacity of ACCA to efficiently inhibit the growth of wild-type and mutant p53 breast carcinoma cells, 20590636 supports the possibility that ACCA may prove efficacious in the treatment of human breast and other cancers. Additionally, it is important to note that the cell viability and proliferation in immortal normal human breast epithelial cells were not significantly altered by ACCA at concentrations ranging from 25 to 200 uM, which significantly induced cell death in breast carcinoma cells. Furthermore, our results showed that ACCA significantly inhibited both migration, invasion and in vivo tumor growth of MDA-231 cells. These data together with previous studies demonstrating similar anti-proliferative effects of a-cyano-4-hydroxycinnamate throug
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