PURPOSE: Every year more than 2 million cases of colon cancer are detected across the world. There is a pressing need for identification of efficient therapeutic targets for the management of this disease. Herein, we explored the role of miR-31 in colon cancer via regulation of paired box 6 (PAX6). METHODS: The expression profile of miR-31 was determined by qRT-PCR. Cell viability was determined by qRT-PCR. Colony formation potential was assessed by clonogenic assay. Transwell assay was used for the assessment of the cell migration and invasion. Protein expression was determined by western blot analysis. RESULTS: The findings showed that miR-31 is significantly suppressed in colon cancer. Restoration of the miR-31 in RKO colon cancer cells resulted in significant decline in their viability and colony formation. Conversely, inhibition of miR-31 resulted in the promotion of proliferation and colony formation of the RKO cells. The miR-31 overexpression also caused a remarkable decrease in the migration and invasion potential of the RKO cells. Bioinformatic approaches showed that PAX6 acts as the target of miR-31 in colon cancer and the interaction between these two also confirmed by dual-luciferase assay. The expression of PAX6 was found to be significantly upregulated in colon cancer cells and miR-31 overexpression suppressed its expression. Additionally, PAX6 silencing resulted in decline in the RKO cell viability. However, PAX6 overexpression promoted the proliferation of RKO cells by avoiding the tumor suppressive effects of miR-31. CONCLUSION: Taken all together, miR-31 may prove essential therapeutic target for the treatment of colon cancer.
PURPOSE: Every year more than 2 million cases of colon cancer are detected across the world. There is a pressing need for identification of efficient therapeutic targets for the management of this disease. Herein, we explored the role of miR-31 in colon cancer via regulation of paired box 6 (PAX6). METHODS: The expression profile of miR-31 was determined by qRT-PCR. Cell viability was determined by qRT-PCR. Colony formation potential was assessed by clonogenic assay. Transwell assay was used for the assessment of the cell migration and invasion. Protein expression was determined by western blot analysis. RESULTS: The findings showed that miR-31 is significantly suppressed in colon cancer. Restoration of the miR-31 in RKO colon cancer cells resulted in significant decline in their viability and colony formation. Conversely, inhibition of miR-31 resulted in the promotion of proliferation and colony formation of the RKO cells. The miR-31 overexpression also caused a remarkable decrease in the migration and invasion potential of the RKO cells. Bioinformatic approaches showed that PAX6 acts as the target of miR-31 in colon cancer and the interaction between these two also confirmed by dual-luciferase assay. The expression of PAX6 was found to be significantly upregulated in colon cancer cells and miR-31 overexpression suppressed its expression. Additionally, PAX6 silencing resulted in decline in the RKO cell viability. However, PAX6 overexpression promoted the proliferation of RKO cells by avoiding the tumor suppressive effects of miR-31. CONCLUSION: Taken all together, miR-31 may prove essential therapeutic target for the treatment of colon cancer.