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The results from study indicate that the anti-proliferative activity is in part due to inhibition of cyclin-mediated gene expression. This effect is further supported by an analysis of cyclin-dependent kinase (CDK)-positive CDK4 (CDK4 or cyclin-D1) mRNA and cyclin-dependent kinase (CDK5). In addition, anti-proliferative effect of terbinafine was observed as it reduced the expression of cyclin-dependent kinase 2 (cdk-2) mRNA. To confirm this result, we also analysed expression of cyclin-dependent phosphoinositide-3-kinase (CDK)2, and cdk4 cdk5, both of which were expressed in colon cancer tissue and cell lines from patients a case-control study. In the sample anti-proliferative effect of terbinafine was not detected, even in the CDK2-positive colon cancer (CCD2064) cells (Figure 3).
Figure 3 Expression of cyclin-dependent kinase 2, cdk4 and cdk5 in CCD2064 colon cancer cells. A: The ratio of gene expression values in different cell lines after treatment of cells with terbinafine and the corresponding control is shown in the graph. Data of 10 clones were used in the control group. * P value < 0.05 relative to control. B and C: The results from experiment of CCD2064 cells patient T, treatment with terbinafine resulted in a marked induction of anti-proliferative activity as demonstrated by reduced expression of the cyclin-dependent kinase 2 (cdk2) and phosphoinositide 3-kinase (cdk5), as shown in the graph. genes significantly induced by terbinafine were cyclin-dependent kinase 2 (CDK2), 3 (CDK3) and cdk5. CDK2, cyclin-dependent kinase 2; CDK3, 3; cdk5, cyclin-dependent phosphoinositide 5-kinase; CCD2064, colon adenocarcinoma cell line and case control; p-nucleotide, p-nitrophenol. Full size image Download PowerPoint slide
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this study there were several interesting results observed that indicate the potential therapeutic applications of terbinafine for the treatment colorectal cancer. One of the main features anti-proliferative effect of terbinafine is its inhibition DNA synthesis and degradation. In the present study we were able to demonstrate that terbinafine reduces the proliferation of colon cancer cells by the inhibition of DNA synthesis, and its anti-proliferative effect can be partly ascribed to the inhibition of both p53 and the cyclin-dependent kinase 2 kinase. We showed that terbinafine inhibited the growth and survival of colon cancer cells, and this effect was associated with reduced levels of cyclin D2 and D1.
Further evidence supporting terbinafine efficacy is provided by the results from a study terbinafine tablets buy uk
of the efficacy terbinafine in other tumors. After treating mice with terbinafine, the incidence of neoplasms similar to colon cancer were significantly reduced. We have shown that the treatment with terbinafine caused a terbinafine buy uk marked reduction in the incidence of adenocarcinoma (Figure 4a). In this study the level of cyclin-dependent kinase 2 (CDK2) has been analyzed with the use of PCR-Agarose and Western blotting techniques (Figure 4b). These methods indicate significantly less levels of cyclin-dependent kin.
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