Background: The present study aimed to investigate the expression, function and clinical implication of zinc finger protein 750 (ZNF750) in colonic cancer and explore the mechanism of its dysregulation.
Methods: The expression of ZNF750 in 76 pairs of colonic cancer tissues was determined using immunohistochemistry. The expression of ZNF750 in colonic cancer cells was detected using western blotting. The correlation between the expression level of ZNF750 and clinicopathological parameters in patients with colonic cancer was analyzed using a chi-squared test. CCK-8 and colony formation assays were used to monitor cell proliferation. Additionally, flow cytometry was used to detect apoptosis of cells; scratch healing and Transwell assays were conducted to evaluate the migration and invasion of cells. Ultimately, the binding relationship between miR-17-5p and ZNF750 was validated using western blotting, a real-time polymerase chaub reaction and a dual-luciferase reporter gene assay.
Results: The expression level of ZNF750 in colonic cancer tissues, as well as colonic cancer cell lines, was significantly down-regulated. Low expression of ZNF750 was associated with larger tumor size and poor tumor differentiation. The over-expression of ZNF750 inhibited the proliferation, motility and invasion but promoted the apoptosis of colonic cancer cells. After the cells were transfected with miR-17-5p mimics, the expression of ZNF750 at both mRNA and protein levels was markedly decreased, whereas the expression of ZNF750 was markedly increased after transfection of miR-17-5p inhibitors. MiR-17-5p could suppresses the malignant biological behaviors via negatively regulating ZNF750.
Conclusions: ZNF750 is negatively regulated by miR-17-5p and inhibits the progression of colonic cancer.
Keywords: ZNF750; colonic cancer; invasion; miR-17-5; proliferation.
© 2020 John Wiley & Sons, Ltd.