Metformin also decreased the expression of CSC markers,CD44, EpCAM,EZH2, Notch-1, Nanog and Oct4, and caused reexpression of miRNAs (let-7a,let-7b, miR-26a, miR-101, miR-200b, and miR-200c) that are typically lost in pancreatic cancer and especially in pancreatospheres.
The expression of let-7c, let-7f, and miR-200c were significantly reduced in most patients whereas the expression of miR-486-5p and miR-451 were significantly elevated in all pancreas cancer patients.
These data suggest that, in addition to regulating proteins that modulate EMT, miR-200c influences expression of cell surface mucins in pancreatic cancer.
The node degree of hsa-miR-200c, hsa-miR-429, and hsa-miR-200b (miRNA), and EFNB2, MYRIP, and PHF17 (mRNA) were extremely high in the miRNA-mRNA network, indicating that these miRNA and mRNA may play a key role in the development of pancreatic cancer.
The goal of this study was to investigate the effect of miRNA-200c (miR-200c) on the EMT, tumorigenesis, colony formation, invasion and chemoresistance of human pancreatic cancer stem cells (PCSCs).
The goal of this study was to investigate the role of miRNA-200c (miR-200c) in regulating colony formation, invasion and chemoresistance of human pancreatic cancer stem cells (PCSCs).