Restoration of miR-200 expression suppresses proliferation and mobility of pancreatic cancer cell.

A number of various human malignancies have been associated with abnormal microRNAs (miRNA) expression. There are evidence that miR-200 operates as both tumor suppressor and an onco-miR in a variety of tumors. In this study, we evaluated the effects of miR-200 on the proliferation and migration of pancreatic cancer cells, as well as the underlying molecular pathways. Clinical tissue samples were used to investigate the expression of miR-200 in pancreatic cancer and normal tissues, and the gene expression omnibus (GEO) database provided bioinformatics confirmation. Using the pCMV vector, miR-200 was transfected into PANC-1 pancreatic cancer cells. After transfection, expression of cancer-related genes (at the mRNA and protein levels) was evaluated. The miR-200-transfected pancreatic cancer cells' survival, invasion, migration, and apoptosis were also investigated. According to the bioinformatics analysis, decreased miR-200 expression was associated with a worse prognosis in pancreatic cancer patients. Moreover, low levels of miR-200 in pancreatic cancer tissues were approved. After transfection, pancreatic cancer cells exhibit a sustained increase in expression of miR-200, which inhibits cell viability, invasion, and migration. Additional investigations revealed that increasing expression of miR-200 increases the proportion of pancreatic cancer cells that endure apoptosis. Changes in the mRNA and protein expression of apoptosis- and metastasis-related genes may account for these findings. Our results indicate that miR-200 functions as a tumor suppressor in pancreatic cancer cells and that upregulating miR-200 levels may be a useful therapeutic strategy for pancreatic cancer patients to halt the progression of the illness.