Calcusyn software help
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This increase has been attributed to a combination of environmental and genetic factors in the general population. Therefore, targeting of these pathways simultaneously with sub toxic doses of pharmacological inhibitors can be a potential therapeutic approach for the treatment of this subset of CRC.ĭespite increased awareness in the general population regarding colorectal cancer (CRC), it still remains a major cause of mortality and morbidity worldwide. These findings demonstrate that co-expression of Cox-2 and FoxM1 might play a critical role in the pathogenesis of CRC. Finally, treatment of CRC xenograft tumors in nude mice with combination of Cox-2 and FoxM1 inhibitors inhibited tumor growth significantly via down-regulation of Cox-2 and FoxM1 expression. In addition, there was also inhibition of cell viability and induction of apoptosis via the mitochondrial apoptotic pathway in CRC cell lines. In vitro, inhibition of FoxM1 and Cox-2 with pharmacological inhibitors Thiostrepton and NS398 resulted in efficient down-regulation of FoxM1 and Cox-2 expression along with in-activation of AKT and inhibition of colony formation, invasion and migratory capability of CRC cells. ResultsĬo-expression of Cox-2 and FoxM1 was detected in 33.3 % (232/697) of CRC’s and associated with an aggressive phenotype characterized by younger age ( p = 0.0191), high proliferative index marker Ki-67 ( p = 0.004) and MMP-9 ( p = 0.0116) as well as activation of AKT ( p = 0.0214). Calcusyn software was utilized to estimate the synergistic doses using chou and Talalay method. Immunoblotting was performed to examine the expression of proteins. Apoptosis was measured by annexin V/PI dual staining. Cell death was measured using live dead assay. Protein expression of Cox-2 and FoxM1 was determined in a large cohort of 770 clinical CRC samples in a tissue micro-array format by immunohistochemistry. In this study we investigated co-expression of Cox-2 and FoxM1 in a cohort of colorectal carcinoma (CRC) samples and also examined whether inhibition of Cox-2 and FoxM1 simultaneously can lead to inhibition of cell viability and induction of apoptosis in colorectal cancer cell lines and in vivo xenografts. Therefore targeting of these deregulated pathways simultaneously can result in efficient cell death of cancer cells. These cancers cells become more aggressive and quickly develop resistance to therapy. Cross-talk between deregulated signaling pathways in cancer cells causes uncontrolled growth and proliferation.