Emodin inhibits pancreatic cancer EMT and invasion by up-regulating microRNA-1271

Emodin has a direct inhibitory effect on the growth and metastasis of a variety of malignant tumor cells. MicroRNA-1271 (miR-1271) has an extensive tumor-suppression effect by inhibiting epithelial mesenchymal transition (EMT) in tumor cells and induces tumor cell apoptosis. Proceeding with the EMT regulatory mechanism of pancreatic carcinoma, the present study aimed to examine the inhibitory effect of miR-1271 and emodin against invasion and metastasis of pancreatic carcinoma. The expression of EMT-related markers (E-cadherin, ZEB1 and TWIST1) was analyzed by western blotting. mRNA levels of miR-1271, E-cadherin, ZEB1 and TWIST1 in pancreatic tumor cells (SW1990) were measured through reverse transcription-quantitative polymerase chain reaction and cell invasiveness was detected using Transwell assays. In addition, a liver metastatic model was established with an implantation of pancreatic tumor tissue into the spleens of nude mice to study the effect of emodin on pancreatic cancer liver metastasis. In the present study, it was demonstrated that miR-1271 significantly decreased in pancreatic cancer cells and tissues. Twist1 may be a target gene of miR-1271. Emodin could inhibit the proliferation ability of pancreatic cancer cells and increased miR-1271 expression level. Further, we found that miR-1271 significantly inhibited SW1990 cell EMT and invasive ability. We also provided the evidence that emodin inhibited SW1990 cell EMT by raising the level of miR-1271. Moreover, the in vivo experiments have verified the inhibiting effect of emodin against liver metastasis of pancreatic cancer. The data in the present study indicated that emodin inhibited pancreatic cancer EMT and invasion by increasing the content of miR-1271.