We have recently become aware of microRNAs (miRNAs) that appear to play a role in oncogenesis. Some of these miRNAs have the potential to become very promising targets for the development of anticancer therapies. In this study we looked at some of the promising candidates identified in breast cancer; in particular miR-155 and the miR-17-92 cluster. We examined the potential for these targets to be achieved by miRNA silencing techniques. The specific technique we employed in this study is based on the use of antigomirals, or anti-sense miRNA molecules that have been shown to be effective in inhibiting miRNAs. We observed the effects of this potential therapy in the mouse model of breast cancer. The results indicate that for the miR-155 target the therapy is effective. Using luciferal imaging of mice, it was observed that the tumor size was reduced compared to the control. Furthermore, known targets of miR-155 (MAF and SHIP1) were shown to be upregulated compared to the untreated control mouse. Following these results we also performed a micro-array analysis, comparing the gene expression of treated tumor cells with those of non-tumor and untreated tumor cells. From this analysis, several new genes that could interact with mir-155 were identified. Further studies would be needed to determine the nature of these interactions and, importantly, the interactions between them and cancer progression. The mir-17-92 cluster target failed to show the same exuberant results. Compared to control, little or no reduction in tumor growth is observed. No upregulation of mir-17-92 gene targets (E2F1, BIM, and PTEN) was observed. It is unclear why there is a discrepancy between the two goals. Maybe...... middle of paper... which were previously not linked to breast cancer through the use of two-dimensional gel analysis. This study was also able to identify different protein expression patterns from nucleic acid analysis (Wulfkuhle 2002). In another study, Adams and colleagues used a protein biochip to develop a protein expression pattern to differentiate between prostate cancer and benign prostatic hyperplasia. Such studies have paved the way for the discovery of new oncogenic protein markers (Bao-Ling Adam 2002). Through a different approach using biotanylation and mass spectroscopy analysis, another study was able to identify several proteins related to liver metastasis (Borgia 2010). The approaches described above can be applied to our model. Although looking in this direction was beyond the scope of this study, this is the future direction of miR research-155.