The effects of miRNA-1180 on suppression of pancreatic cancer.

The aim of this study was to evaluate the effects of miR-1180 on pancreatic cancer. We sampled adjacent cancer and carcinoma tissues from 30 pancreatic cancer patients and measured miR-1180 expression by qRT-PCR and NF-κB protein expression by immunohistochemistry. To explore the effects of this miRNA in cell culture, we used pancreatic cancer (PANC-1) cells that received only vehicle (negative control, NC), miR-1180 mimic, or miR-1180-inhibitor. Cells were treated with cisplatin to induce apoptosis. Proliferation, apoptosis, cell cycle progression, cell invasion, and cell migration were assessed in the three cell groups. The expression levels of relevant proteins (TNIP2, NF-κB, MMP-2, MMP-9, Bax, Bcl-2, p21, and cyclin D1) in each cell group were determined by western blotting. Compared with healthy tissue adjacent to carcinoma tissues, miR-1180 expression in cancer tissues was significantly enhanced (P<0.05). NF-κB protein had a similar expression pattern to miR-1180; miR-1180 expression was positively correlated with NF-κB expression. The invasion and wound healing abilities of miR-1180-inhibited cells were significantly reduced compared with the NC or miR-1180-expressing cells (P<0.05). The cell proliferation rate of miR-1180-inihibited cells was also significantly lower than that of NC or miR-1180-expressing cells (P<0.05), while the cell apoptosis and G1 phase rates of miR-1180-inihibited cells were significantly higher than the NC or miR-1180-expressing cells (P<0.05). In conclusion, suppressing miR-1180 expression may exert anti-cancer effects on pancreatic cancer cells via regulation of TNIP 2/NF-κB signaling and the downstream MMP-2/-9, Bax, Bcl-2, p21, and cyclin D1 factors.